The endocrine system is a system of endocrine glands with its complex regulation, hierarchy, and complex of relationships between organs. The endocrine system of the body as a whole maintains the constancy in the internal environment necessary for the normal course of physiological processes. In addition, the endocrine system, together with the nervous and immune systems, ensures reproductive function, growth and development of the body, formation, utilization and storage (“in reserve” in the form of glycogen or fatty tissue) of energy. The role of signals in this system is played by hormones.
Hormones are biological active substances that have a strictly specific and selective effect, capable of changing the level of vital activity of the body. All hormones are divided into:
- Steroid hormones - are produced from cholesterol in the adrenal cortex, in the gonads.
- Polypeptide hormones - protein hormones (insulin, prolactin, ACTH, etc.)
- Hormones derived from amino acids - adrenaline, norepinephrine, dopamine, etc.
- Hormones derived from fatty acids - prostaglandins.

According to their physiological effects, hormones are divided into:
- Triggers (hormones of the pituitary gland, pineal gland, hypothalamus). Affects other endocrine glands.
- Performers - influence individual processes in tissues and organs.

The physiological action of hormones is aimed at:
1) provision humoral , i.e. carried out through the blood, regulation of biological processes;
2) maintaining the integrity and constancy of the internal environment, harmonious interaction between the cellular components of the body;
3) regulation of the processes of growth, maturation and reproduction.
The organ that responds to this hormone is target organ (effector). The cells of this organ are equipped with receptors.

Hormones regulate the activity of all cells in the body. They affect mental acuity and physical mobility, physique and height, determine hair growth, tone of voice, sex drive and behavior. Thanks to the endocrine system, a person can adapt to strong temperature fluctuations, excess or lack of food, and physical and emotional stress. The study of the physiological action of the endocrine glands made it possible to reveal the secrets of sexual function and the miracle of childbirth, as well as to answer
The question is why some people are tall and others are short, some are plump, others are thin, some are slow, others are agile, some are strong, others are weak.
In a normal state, there is a harmonious balance between the activity of the endocrine glands, the state of the nervous system and the response of target tissues (tissues that are targeted). Any violation in each of these links quickly leads to deviations from the norm. Excessive or insufficient production of hormones causes various diseases, accompanied by profound chemical changes in the body.
He studies the role of hormones in the life of the body and the normal and pathological physiology of the endocrine glands. endocrinology .

Aging and the endocrine system

The aging process is accompanied by numerous dysfunctions of the endocrine system. It is often difficult to determine what is the cause of these disorders - old age itself or the diseases that accompany it.

In older animals, the concentrations of most hormones are reduced. The difference between young and old organisms is even more noticeable when comparing the reactions of the endocrine glands to external influences. Thus, the pituitary gland of old rats responds to the action of releasing factors of the hypothalamus (liberins) by secreting a smaller amount of tropic hormones. By artificially replenishing substances missing in the pituitary gland of old rats, it is possible to delay or reverse the weakening of reproductive function, the development of tumors and the involution of the thymus gland.

Another reason for the weakening of endocrine regulation is age-related changes in the structure of hormones and, accordingly, their activity. Thus, as we age, the molecular weight changes and the activity of thyrotropin (TSH) decreases. By artificially introducing calcium into the cell, in some cases it is possible to prevent a decrease in its response to hormones. This may suggest a new treatment strategy. Changes also occur in the binding of calcium in the cell.

In old age, the formation of catecholamines in the sympathetic part of the autonomic nervous system increases. On the other hand, the effects transmitted by the action of catecholamines on adrenergic receptors are weakened. All this narrows the range of possible responses to extreme environmental influences. Perhaps additional amounts of catecholamines are needed for better utilization of nutrients: by acting on adipocytes, catecholamines enhance lipolysis. They also activate glycogenolysis through liver adrenergic receptors.

In old age, changes occur in the regulation of glucose metabolism. The number of β cells in the pancreas decreases. In response to rising glucose concentrations, they release less insulin into the blood. Feedback, which suppresses the release of glucose by the liver (as its concentration in the blood increases), acts more slowly. Insulin activity decreases, and accordingly, glucose uptake into muscles is impaired. The result of these changes is a decrease in glucose tolerance and sometimes the development of diabetes mellitus.
The connection between aging and the endocrine system is described by Dilman's elevation theory.

Elevation theory of Dilman

In the early 1950s, the famous Russian gerontologist V.M. Dilman put forward and substantiated the idea of ​​the existence of a single regulatory mechanism that determines the patterns of age-related changes in various homeostatic (maintaining the constancy of the internal environment) systems of the body. According to Dilman's hypothesis, the main link in the mechanisms of both development (Latin elevatio - rise, in a figurative sense - development) and subsequent aging of the body is the hypothalamus - the “conductor” of the endocrine system. Some gerontologists, including Dilman, believe that many of the changes that appear in the body as a person ages are due to the body’s gradual loss of the ability to maintain homeostasis through hormonal control and brain regulation. Many symptoms of aging appear to be due to a loss of control over hormone production, resulting in either too much or too little of it being produced and the regulation of life processes becoming unbalanced. Menopause, for example, is caused by the loss of the hormone estrogen produced by the ovaries. This leads to a decrease in fertility and a decrease in vaginal discharge (which can interfere with sexual intercourse), decreased muscle tone, thinning and dry skin. During menopause, the amount of cholesterol and blood increases, which means that after the cessation of menstruation, women are equally at risk of heart disease, which is associated with the fact that cholesterol deposits block the blood supply to the heart. The main cause of aging is an age-related decrease in the sensitivity of the hypothalamus to regulatory signals coming from the nervous system and endocrine glands. Throughout the 1960-80s. With the help of experimental studies and clinical observations, it was established that it is this process that leads to age-related changes in the functions of the reproductive system and the hypothalamic-pituitary-adrenal system, which ensures the necessary level of glucocorticoids produced by the adrenal cortex - “stress hormones”, daily fluctuations in their concentration and increased secretion during stress, and, ultimately, to the development of a state of so-called “hyperadaptosis”. The consequence of similar age-related changes in the metabolic homeostatic system, which regulates appetite and energy supply of body functions, is an increase in body fat content with age, a decrease in tissue sensitivity to insulin (prediabetes) and the development of atherosclerosis.
Endocrine regulation:

An important stage in the development of the elevation theory was the establishment of the role of age-related changes that naturally occur in these three main “superhomeostats” (reproductive, adaptive and metabolic) in the formation of such phenomena that are of key importance for the life expectancy of an individual, such as metabolic immunosuppression and cancrophilia, i.e. . the formation of conditions conducive to the occurrence of malignant neoplasms. Developing and deepening his concept for almost 40 years, V.M. Dilman came to the conclusion that aging (and the main diseases associated with aging) is not programmed, but is a by-product of the implementation of a genetic development program and therefore aging occurs with a pattern inherent in the genetic program. According to Dilman's concept, aging and related diseases are a by-product of the implementation of the genetic program of ontogenesis - the development of the body.
The ontogenetic model of age-related pathology has opened up new approaches to the prevention of premature aging and diseases associated with
age and are the main causes of human death: heart disease, malignant neoplasms, strokes, metabolic immunosuppression, atherosclerosis, diabetes mellitus in the elderly and obesity, mental depression, autoimmune and some other diseases. From the ontogenetic model it follows that the development of diseases and natural senile changes can be slowed down if the state of homeostasis is stabilized at the level achieved by the end of the development of the organism. If you slow down the rate of aging , then, as V.M. believed. Dilman, it is possible to increase the species limits of human life.

Modern ideas about the mechanisms of the geroprotective effect of a calorie-restricted diet, antidiabetic biguanides, pineal peptides and melatonin, some neurotropic drugs (in particular, L-DOPA and the monoamine oxidase inhibitor deprenyl), and succinic acid indicate the promise of this approach.

Unfortunately, there are no articles by Dilman in electronic form yet, but you can read his main work, “The Large Biological Clock.”

Thus, Dilman's theory is a generalization of a group of theories of programmed death. The modern version of Dilman's theory is the neuroendocrine theory. One of the main age-associated disorders is the insensitivity of cells to hormonal stimuli.

Pineal gland and aging mechanisms

Now in the scientific world the expression “The pineal gland is the sundial of the body” has become popular. The most significant phenomenon for living nature on Earth is the change of day and night, light and darkness. Its rotation around its axis and at the same time around the Sun measures the day, seasons and years of our life. More and more information is accumulating about the role of the pineal gland as the main pacemaker of body functions. Light inhibits the production and secretion of melatonin, and therefore its maximum level in the pineal gland and blood in humans and animals of many species is observed at night, and the minimum in the morning and during the day. With aging, the function of the pineal gland decreases, which is manifested primarily by a disturbance in the rhythm of melatonin secretion and a decrease in the level of its secretion (Touitou, 2001; Reiter et al., 2002).
In people in the age group of 60-74 years, most physiological indicators show a positive phase shift in the circadian rhythm (~1.5-2 hours), with its subsequent desynchronization in people over 75 years of age (Gubin, 2001). If the pineal gland is likened to the biological clock of the body, then melatonin can be likened to a pendulum, which ensures the progress of this clock and a decrease in the amplitude of which leads to its stop. Perhaps it would be more accurate to compare the pineal gland with a sundial, in which melatonin plays the role of a shadow from the gnomon - a rod that casts a shadow from the sun. During the day, the sun is high and the shade is short (melatonin levels are minimal), in the middle of the night there is a peak in the synthesis of melatonin by the pineal gland and its secretion into the blood. It is important that melatonin has a daily rhythm, that is, its unit of measurement is the chronological metronome - the daily rotation of the Earth around its axis.
If the pineal gland is the body's sundial, then, obviously, any changes in the length of daylight hours should significantly affect its functions and, ultimately, the rate of its aging. The circadian rhythm is very important not only for the temporal organization of the physiological functions of the body, but also for its life expectancy. It has been established that with age, the neural activity of the suprachiasmatic nucleus decreases, and when kept under constant lighting conditions, these disorders develop faster (Watanabe et al, 1995). Old animals are resistant to the action of clorgyline, which stimulates the biosynthesis of melatonin in conditions of round-the-clock lighting; destruction of the suprachiasmatic nucleus of the hypothalamus has the same effect (Oxenkrug, Requintina, 1998). A number of studies have shown that disruption of photoperiods can lead to a significant reduction in the life expectancy of animals (Pittendrigh and Minis, 1972; Pittendrigh and Daan, 1974).
M. W. Hurd and M. R. Ralph (1998) studied the role of the circadian rhythm in the aging of the body in golden hamsters Mesocricetus auratus with a mutation in the pacemaker tau. The authors received 3 groups of hamsters; having wild type (+/+), homozygotes tau-/tau- and heterozygotes tau-/+, and then their hybrids. Preliminary three-year observations showed that tau-/+ heterozygotes had a 20% lower life expectancy than homozygotes. The lifespan of tau-/+ mutant heterozygotes kept under a 14-hour light/10-hour dark regime was almost 7 months shorter than in the +/+ or tau-/tau- homozygote groups (p< 0.05), однако средняя продолжительность жизни обеих гомозиготных групп была практически одинаковой. При круглосуточном содержании хомячков в условиях постоянного слабого освещения (20- 40 люкс) с 10-недельного возраста средняя продолжительность жизни гетерозигот и гомозигот была одинаковой и колебалась от 15 до 18 месяцев. Для изучения причин влияния циркадного ритма на продолжительность жизни авторы имплантировали в головной мозг старых хомячков супрахиазматические ядра от плодов хомячков различного генотипа. Было установлено, что хомячки с прижившимися имплантатами жили в среднем на 4 месяца дольше, чем интактные или ложнооперированные контрольные животные. Авторы полагают, что результаты их экспериментов свидетельствуют о том, что нарушения циркадного ритма сокращают продолжительность жизни животных, тогда как их восстановление с помощью имплантации фетального супрахиазматического ядра (спонтанного осциллятора) увеличивает ее почти на 20%. Таким же эффектом, по мнению авторов, будут обладать любые воздействия, направленные на нормализацию циркадного ритма. Интересно, что разрушение осциллятора (супрахиазматического ядра) приводит к сокращению продолжительности жизни животных (DeCoursey et al., 2000).

Melatonin and aging

Melatonin is the “night hormone”, a hormone of the pineal gland that regulates circadian rhythms. The main physiological effect of melatonin is to inhibit the secretion of gonadotropins. In addition, the secretion of other tropic hormones of the anterior pituitary gland - corticotropin, thyrotropin, somatotropin - decreases, but to a lesser extent.
The secretion of melatonin is subject to a daily rhythm, which, in turn, determines the rhythm of gonadotropic effects and sexual function. The synthesis and secretion of melatonin depend on illumination - excess light inhibits its formation, and decreased illumination increases the synthesis and secretion of the hormone. In humans, 70% of daily melatonin production occurs at night.

The ability of melatonin to increase the lifespan of mice was first established by W. Pierpaoli and G. J. M. Maestroni (Pierpaoli, Maestroni, 1987). In November 1985, the authors began daily administration of melatonin in drinking water (10 mg/L) to 10 male C57BL/6J mice. 10 control animals received a 0.01% ethanol solution, which served as a solvent for melatonin. At the beginning of the experiment, the mice were 575 days old (about 19 months), and they were all quite healthy. The animals received melatonin from 18.00 to 8.30 hours. 5 months after the start of the experiment, the control animals began to lose weight, were inactive, and went bald. The administration of melatonin protected the animals from age-related weight loss and it remained at the level of 18 months. The average lifespan of mice under the influence of melatonin increased by 20%, amounting to 931 ± 80 days versus 752 ± 81 in the control group. According to the authors’ calculations, the difference is significant (p 0.05).
In 1991, W. Pierpaoli et al. (1991) presented the results of three series of experiments with chronic administration of melatonin to mice of different strains. In all experiments, melatonin was administered only at night with drinking water (10 mg/l). Melatonin was administered to 15 female SZN/He mice at 12 months of age. There were 14 mice in the control group. Melatonin not only did not increase the life expectancy of these mice, but led to an increase in the frequency of development of neoplasms, mainly affecting the organs of the reproductive system (lympho- or reticulosarcoma, ovarian carcinoma). Data on average life expectancy and the incidence of neoplasms in the control and experimental groups were not provided. It should be noted that female SZN/He mice are characterized by a high incidence of spontaneous mammary tumors (Storer, 1966), but the authors do not report any information about their detection in the control or experimental groups. Mice treated with melatonin lived on average 2 months less than controls.
In the 2nd series of experiments, melatonin was administered during the day or night to female NZB (New Zealand Black) mice, characterized by a high incidence of autoimmune hemolytic anemia, nephrosclerosis and systemic or localized reticulocellular tumors of type A or B. There were 10 in each group animals, and melatonin was started to be administered at four months of age. The administration of melatonin during the day had no effect on the survival of mice, and all of them died by 20 months of age (in the control - by the 19th month of life). When melatonin was administered at night, 4 out of 10 mice in this group were alive at the age of 20 months, and 2 mice survived to 22 months of age. The last mouse lived for 2 months, that is, 4 months longer than the maximum life expectancy in the control group. The authors did not observe any differences in causes of death in the control and experimental groups.
The 3rd series of experiments was a repetition of the experiment with male mice of the C57BL/6 line. This time there were 20 mice in the control group and 15 mice in the experimental group at the age of 19 months. The average life expectancy in the control group was 743 ± 84 days, and in the group receiving melatonin - 871 ± 118 days (p0.05 when calculated using Student's t test). The administration of melatonin did not significantly affect the body weight of mice in one direction or another when compared with the control.
Later, W. Pierpaoli and W. Regelson (1994) summarized the old data and presented the results of new experiments studying the effect of melatonin on the lifespan of mice of different strains. Melatonin was administered with drinking water (10 mg/l) at night (from 18:00 to 8:30). Female BALB/c mice began receiving the hormone at 15 months of age. The average lifespan of the 26 control animals was 715 days, while the 12 melatonin-treated mice lived an average of 843 days, or 18% longer. The median was 24.8 months in the control group and 28.1 months in the experimental group, respectively, and the maximum life expectancy was 27.2 and 29.4 months, respectively. The authors did not observe any differences in body weight between the mice in both groups. In another experiment, melatonin was also administered through drinking water at night at a dose of 10 mg/l to male BALB/c mice starting at 18 months of age and killed in groups 4, 7 and 8 months after the start of exposure. After 8 months of observation, the weight of the thymus, adrenal glands and testicles of mice treated with melatonin was significantly different from age-matched controls. Similarly, indicators such as the number of lymphocytes in peripheral blood, the level of zinc, testosterone and thyroid hormones improved. The authors believe that cyclic administration of melatonin has a positive effect on mice, maintaining a more youthful state of endocrine and thymic-lymphoid organs in them. It should be noted that the number of old mice in the groups was extremely small (5-6), and the control group of 3-month-old mice included only 3 animals.
S. P. Lenz et al. (1995) administered melatonin to female NZB/W mice in a single dose of 100 μg per mouse (2-3.5 mg/kg) daily in the morning (between 08.00 and 10.00 h) or in the evening (between 17.00 and 19.00 h) starting at eight months. age and for 9 months. There were 15 animals in each group. It was found that the administration of melatonin in the morning is significant (p<0.001) увеличивает выживаемость мышей, тогда как вечерние инъекции таким эффектом не обладали. Так, если до 34-недельного возраста дожило только 20 % контрольных мышей, в "утренней" группе были живы 65% животных, причем 30% дожили до конца периода наблюдения (44 недели). В "вечерней" группе до 34-недельного возраста дожило практически столько же (60%) мышей, однако 37-недельный возраст пережили лишь 20% животных. Авторы отметили замедление возрастного нарастания протеинурии у мышей, которым мелатонин вводили в утренние часы. К сожалению, наблюдение за животными было прекращено до естественной гибели животных во всех группах. Число мышей в группах было весьма невелико, полная аутопсия животных не производилась.
E. Mocchegiani et al. (1998) administered melatonin in drinking water (10 g/l) at night to 50 male Balb/c mice starting at 18 months of age. 50 mice of another group received water with the addition of zinc sulfate (22 mg/l) and 50 served as intact controls. The mice were monitored until natural death and were regularly weighed and food intake determined. The use of melatonin and zinc significantly shifted the survival curves of animals to the right and increased the maximum life expectancy of animals by 2 and 3 months, respectively, compared to the intact control. Neither melatonin nor zinc affected feed intake and body weight dynamics of animals.
A. Conti and G. J. M. Maestroni (1998) studied the effect of melatonin on the lifespan of female NOD (non-obese diabetic) mice, characterized by a high incidence of insulin-dependent diabetes. One of the groups of mice (n = 25) underwent epiphysectomy immediately after birth, the 2nd group (n = 30) received melatonin subcutaneously at a dose of 4 mg/kg at 16.30 hours 5 times a week from the age of 4 weeks until 38. th week of life. Mice of the 3rd group were injected with bovine serum (PBS) subcutaneously according to the same regimen, and they served as a control for group 2. Mice of the 4th group (n = 17) were administered melatonin with drinking water (10 mg/l) at night 5 once a week from the 4th to the 38th week of life; The 5th group consisted of 29 intact animals. Epiphysectomized mice began to die already at the age of 19 weeks; their autoimmune diabetes rapidly progressed, and by the 32nd week of life, 92% of all animals in this group died. In the control mice began to die from the 18th week of life, but the slope of the survival curve was significantly less and by the 50th week of life 65.5% of the control animals died. Chronic subcutaneous administration of melatonin for 33 weeks significantly slowed the rate of disease progression and reduced mortality. Only 10% of mice given subcutaneous melatonin did not survive to 50 weeks of age. Interestingly, bovine serum injections also slowed the development of diabetes, but only 32% of mice in this group survived to 50 weeks of age. The effect of melatonin administration with drinking water was less pronounced than with its subcutaneous administration: 58.8% of mice in this group survived to the end of the observation period versus 34.5% in the control (p<0.0019). Таким образом, если эпифизэктомия ускоряла развитие диабета и укорачивала продолжительность жизни мышей линии NOD, то введение мелатонина замедляло развитие заболевания и увеличивало продолжительность жизни животных (Conti, Maestroni, 1998).
In another large study, dietary melatonin (11 ppm or 68 μg/kg body weight per day) was administered to male C57BL/6 mice starting at 18 months of age (Lipman et al., 1998). The dynamics of body weight and food consumption under the influence of melatonin did not differ significantly from those in control animals. There were also no differences in mortality between control mice and mice fed melatonin. Thus, 50% mortality in the control group occurred at the age of 26.5 months, and with the introduction of melatonin - at 26.7 months. Mortality curves, as well as data on the maximum life expectancy of animals in different groups, are not presented in the work. Moreover, they were killed at the age of 24 months (cohort 1) or at the age when half of all animals in the group died (age of 50% mortality), that is, 6 or 8.5 months after the start of the experiment (cohort 2). The last, 3rd cohort consisted of mice that died before the age of two years or before reaching the age of 50% mortality. The first cohort included 20 control and melatonin-treated mice, the second, 7 and 13 mice, respectively, and the third, 38 and 30 animals, respectively. In these three cohorts, the incidence of developing pathological processes was assessed separately. The authors did not find any differences in the overall incidence of pathological processes between control and melatonin-treated mice. However, such a conclusion, in our opinion, is not entirely correct and is refuted by the data presented in the article. Thus, the authors united under one heading all pathological processes, including degenerative-atrophic, lymphoproliferative, and neoplasms. However, if the frequency of lymphomas among mice of the control group and the group receiving melatonin (3rd cohort) was the same (21.1 and 23.3%, respectively), then among those who survived to the 50% mortality rate it was 28.6 and 77.9%, respectively. It is extremely surprising that there is no mention of lymphomas in mice in the 1st cohort, that is, those killed at the age of 24 months, which is only 2.5-3 months less than in cohort 2, despite the fact that in those that died before this period, lymphomas were detected at 21-23% of cases. The article completely lacks information about neoplasms of other localizations in mice of different groups. We have to admit that the work of Lipman et al. (1998) contains a number of serious methodological errors that call into question the results of the entire work and its conclusions.
In Anisimov’s experiments (Anisimov et al., 2001), 50 experimental female CBA mice, starting from the age of six months, were administered melatonin (20 mg/l) in drinking water in courses (5 days in a row once a month). 50 intact females served as controls. The animals were observed until their natural death. The mice were weighed monthly and the amount of food consumed was determined. Every three months, estrous function, muscle strength, fatigue, and locomotor activity of the mice were examined, and body temperature was measured. All animals were necropsied. The detected tumors were examined histologically. It was found that long-term administration of melatonin to female CBA mice slowed down age-related changes in estrous function and did not have any adverse effect on their physical activity. During the experiment, it was found that the body temperature of mice in the control group did not fall, and in the 9th month of the experiment it was significantly higher compared to the 6th month. In mice receiving melatonin, on the contrary, body temperature significantly decreased throughout the experiment (p< 0.001). Сходная тенденция отмечена также при измерении средней температуры отдельных фаз эстрального цикла. Однако различий между значениями температуры отдельных фаз цикла практически не было. Только у мышей подопытной группы на 3-м месяце опыта температура во время эструса была достоверно выше, чем во время метаэструса и проэструса (р < 0.05).
Based on the data on the effect of melatonin on the lifespan of mice, it can be seen that the dynamics of survival did not differ in both groups until the age of 22 months, after which a clear decrease in mortality was observed under the influence of melatonin. While not a single control mouse remained alive by the age of two years, there were 9 mice treated with melatonin. Thus, the survival curve of mice treated with melatonin was shifted to the right compared to the survival curve of control mice. The average lifespan of mice in both groups did not differ significantly, while the maximum lifespan under the influence of melatonin increased by almost 2.5 months.
Thus, the use of melatonin had a certain enhancing effect on spontaneous carcinogenesis in female CBA mice. The number of mice with malignant tumors in the experimental group was significantly (20%) higher than in the control group. Under the influence of melatonin, the appearance of 4 leukemias and 5 adenocarcinomas of the lungs was noted (p<0.01), отсутствовавших в контрольной группе. Показано наличие опухолей матки в подопытной группе мышей. Однако под влиянием мелатонина у мышей реже развивались аденомы легких (в 2.5 раза, р<0.001). Не наблюдалось существенного влияния мелатонина на развитие новообразований какой-либо иной локализации.
In the same article, Anisimov proposed an aging-antiaging scheme, in which melatonin also plays a certain role:


In experiments on SHR females, melatonin was also administered with drinking water at night in two doses (2 and 20 mg/l), for 5 consecutive days monthly, starting from the age of the 3rd month (Anisimov et al., 2003). The use of melatonin was accompanied by a slowdown in the age-related switching off of estrous function, a slight decrease in body weight (in a small dose) and an increase in the average life expectancy of the last 10% of mice. Melatonin at a dose of 2 mg/l significantly inhibited the development of tumors in mice of this line (1.9 times compared with the intact control). At the same time, the most pronounced effect was observed in relation to adenocarcinomas of the mammary gland, the frequency of which decreased by 4.3 times.
Thus, information about the effect of melatonin on life expectancy and the development of spontaneous tumors in mice of various strains is quite contradictory.
If we do not take into account the experiments of V.I. Romanenko, in which melatonin was administered in a very large dose, it turns out that when administered to mice of different strains and regardless of the time of start of use, melatonin increased the average life expectancy in 12 experiments out of 20 and in 8 had no effect. When dividing animals by sex, it turned out that melatonin showed a geroprotective effect in 4 out of 5 experiments performed on males, while in females only in 8 out of 15 experiments a positive result was obtained. In 8 of 14 experiments in which melatonin was administered at a relatively young age (up to 6 months), the result was positive and in 6 there was no effect. It should be noted that most of the described experiments were performed on a small number of animals, which, of course, reduces the reliability of the results obtained in such experiments. It should be noted that in 4 series of experiments in which there were a sufficient number of animals (50 in each group), three gave a positive result, that is melatonin had a geroprotective effect.

Of course, experiments to study the role of melatonin in the aging process will continue.

Insulin is a hormone that regulates metabolism. In recent years, cardiovascular diseases have taken first place in mortality. And they are directly related to insulin imbalance. Developing , poetically called by scientists the “quadriga of death.” According to modern concepts, the unifying basis of all manifestations of metabolic syndrome is primary insulin resistance and concomitant systemic hyperinsulinemia (increased insulin levels in the blood). Hyperinsulinemia, on the one hand, is compensatory, that is, necessary to overcome insulin resistance and maintain normal glucose transport into cells; on the other hand, pathological, contributing to the emergence and development of metabolic, hemodynamic and organ disorders, ultimately leading to the development of type 2 diabetes mellitus, coronary artery disease and other manifestations of atherosclerosis. This has been proven by a large number of experimental and clinical studies.

To date, all possible causes and mechanisms for the development of insulin resistance in abdominal obesity have not been fully studied; not all components of the metabolic syndrome can be clearly linked and explained by insulin resistance. The modern understanding of the causes of the syndrome is represented by the following diagram:

Insulin resistance is a decrease in the response of insulin-sensitive tissues to insulin when its concentration is sufficient. The study of genetic factors responsible for the development of insulin resistance has shown its polygenic nature. In the development of insulin sensitivity disorders, mutations in the genes for insulin receptor substrate (ISR-1), glycogen synthetase, hormone-sensitive lipase, b3-adrenergic receptors, tumor necrosis factor-a, uncoupling protein (UCP-1), as well as molecular defects in proteins that transmit insulin signals (increased expression of Rad protein and UPC-1 insulin receptor tyrosine kinase inhibitor in muscle tissue, decreased membrane concentration and activity of intracellular glucose transporters GLUT-4 in muscle tissue).

An important role in the development and progression of insulin resistance and associated metabolic disorders is played by abdominal adipose tissue, neurohormonal disorders accompanying abdominal obesity, and increased activity of the sympathetic nervous system.
Hormonal disorders accompanying visceral-abdominal obesity:
- increased cortisol
- increase testosterone and androstenedione in women
- decreased progesterone
- decreased testosterone in men
- decrease in somatotropic hormone
- increase in insulin
- increased norepinephrine
Hormonal disorders primarily contribute to the deposition of fat mainly in the visceral area, as well as directly or indirectly to the development of insulin resistance and metabolic disorders.
A complex cascade of reactions leads to the emergence and development of age-associated diseases and death.

The article by Japanese scientists from Keio University School of Medicine, “Metabolic syndrome, IGF-1 and insulin action,” discusses all these issues in detail.

Insulin paradox

One of the groups of age-associated diseases, various neurodegenerative diseases have different times of manifestation, and different proteins are involved in their development. Familial forms of the disease manifest themselves in the fifth decade of life, sporadic cases after 70 years. Until recently, the relationship between the aging process and toxic protein aggregation (a common feature of neurodegenerative diseases) was unclear. The insulin and insulin-like growth factor 1 (IGF1) signaling pathway regulates lifespan, metabolism, and stress resistance and is associated with neurodegenerative diseases and the aging process. Loss of this pathway results in diabetes, but may result in increased lifespan and decreased aggregation of toxic proteins. In a recent paper by Cohen E and Dillin A of The Salk Institute for Biological Studies, "The Insulin Paradox: Aging, Protein Toxicity, and Neurodegenerative Diseases," the authors discuss this paradox and the therapeutic potential of targeting this signaling pathway to treat neurodegenerative diseases.

Age and hormone-associated cancer

As is known, the incidence of cancer increases with age. Hormone-associated tumor types are considered age-associated - prostate cancer, breast cancer, uterine adenocarcinoma, ovarian cancer, pancreatic cancer and thyroid cancer. Let's look at the most common adult cancer - breast cancer. In women, breast cancer is at least 100 times more common than in men, which has long forced researchers to recognize that assessing the state of the reproductive system is one of the important approaches to studying the pathogenesis of this tumor. This, in particular, is reflected in the fact that among the risk factors for breast cancer, the significance of which has been confirmed by multiple and multicenter epidemiological studies, along with the presence of the same disease in blood relatives and previous biopsies for benign processes in the gland, early onset of menarche is represented , late menopause and late first birth. (On this basis, a number of models have been built for predicting in digital terms the individual risk of developing the disease in “carriers” of the listed stigmata - Gail et al., 1989.) However, it must be emphasized that if the combination of early first menstruation and late menopause is, in particular, a reflection longer reproductive period (and, accordingly, longer hormonal stimulation of the mammary gland), then late first birth, as a rule, is regarded from a different perspective - delayed completion of full functional maturation of the organ. In this regard, it is emphasized that the differentiation of the cellular elements of the mammary gland, starting from adolescence, reaches its peak after the first birth and lactation, followed by regression during menopause. An important characteristic of these changes is the ratio of primitive ducts, classified as lobules 1 and 2, and differentiated glandular structures (lobules 3 and 4), which together constitute the so-called. terminal ductal-lobular units. It is believed that the higher level of proliferation in lobules 1 and 2 is a result of their higher sensitivity to hormonal stimulation, and, as a consequence, signs of atypia or carcinoma in situ are found in these lobules more often than in lobules 3 and 4 (Russo, Russo , 1997). In these examples, one can see the intersection of several “vectors,” in particular, what should be the state of the target tissue, what hormones are capable of exerting a problastomogenic effect on it, and at what age they act most effectively in this regard (i.e. promote cell degeneration). With regard to the last issue, considerable attention is currently paid to the perinatal and especially the intrauterine period of life. It is assumed that at this moment, peculiar stem cells are “selected” that are least resistant to adverse hormonal influences in utero and are capable of subsequently, subject to hormonal stimulation in adulthood, acquiring the features of true tumor cells (Adami et al., 1995). At the same time, markers of pre-/perinatal predisposition to the development of breast cancer are birth with a large mass, jaundice of newborns, absence of toxicosis of pregnancy, etc., and their true equivalents, possibly important in the pathogenesis of the disease, are excessive intrauterine production of estrogens and growth factors such as IGF-1 (Michels et al., 1996; Berstein, 1997; Ekbom et al., 1997). The influence of these hormones and hormone-like factors can be more rapid or, conversely, delayed, creating conditions for the emergence of various pathogenetic variants of breast cancer and confirming the importance of the age-related (temporary) factor in this disease (Semiglazov, 1980, Semiglazov, 1997; Dilman, 1987 ). The clinical reflection of this situation is, first of all, the existence of pre- and postmenopausal forms of breast cancer and two more or less clear age-related peaks in incidence, separated by about a decade in time. Pre- and postmenopausal variants of the disease differ not only in a number of clinical features, but also in the frequency of detection of certain epidemiological risk factors, and the spectrum of hormonal and metabolic disorders. A typical example is the role of excess body weight and differences in its composition (in the fat/lean mass ratio) for the same body weight: greater weight and an increase in the proportion of fat in the body increase the risk of developing postmenopausal breast cancer and, conversely, " protect" from the occurrence of its premenopausal variant (Bershtein, 1997). Obesity is characterized by deviations in various endocrine homeostats, and accordingly, insulin resistance is one of those parameters that, along with disturbances in steroid production, is currently regarded as one of the leading predisposition factors to the development of breast cancer (Bruning et al., 1992; Gamayunova et al. ., 1987). The difference between insulin and IGF-1 in this regard is that excess IGF-1 in circulation has been prospectively observed to predispose to premenopausal breast cancer (Hankinson et al. , 1998), while hyperinsulinemia and insulin resistance increase the risk of developing both forms of the disease (Bruning et al., 1992). The accelerated growth of the body in length during puberty also acts similarly to the last two factors (Berkey et al., 1999).

Turning again to steroids, it should be noted that the increased risk of breast cancer is determined not only by estrogens and their excessive stimulation of the target tissue. According to some data, the increase in the incidence of breast cancer in women treated with a combination of estrogens and progestins during menopause is almost the same as in women treated with estrogens only, or even higher than in the latter (Schairer et al., 2000); this is consistent with the idea that progesterone has a mitogenic effect on mammary epithelium (Pike, 1987; Henderson et al., 1997). The association of androgens with the same problem appears in two main respects: the risk of developing breast cancer, according to some, but not all, available prospective studies, is contributed, on the one hand, to a decrease in the production of adrenal androgens, in particular dehydroepiandrosterone sulfate (which coincides with previous conclusions about the significance of the so-called Bulbrook discriminant - Bulbrook et al., 1971, and on the other - an excess of predominantly gonadal androgens such as testosterone (Cauley et al., 1999).It is possible that the noted, although variable, multidirectional changes may be due to the different influence of insulin on the production of androgens in the gonads and adrenal cortex, which, in turn, is additional evidence of the combined involvement of steroid and peptide hormones in the analyzed process.Another confirmation of this is the recently presented results of prospective observations, in which a directly proportional relationship is observed between plasma prolactin levels and subsequent breast cancer development (Hankinson et al., 1999).
In a recent paper by Svetlana Ukraintseva et al. from the Center for Population Health and Aging 5) Hormonal aspects of age-associated diseases and many others.

The integration of cells, tissues and organs into a single human body, its adaptation to various changes in the external environment or the needs of the body itself is carried out through nervous and humoral regulation. The neurohumoral regulation system is a single, closely related mechanism. The connection between the nervous and humoral regulatory systems is clearly visible in the following examples.

Firstly, the nature of bioelectric processes is physicochemical, i.e. consists of transmembrane movements of ions. Secondly, the transfer of excitation from one nerve cell to another or an executive organ occurs through a mediator. And finally, the closest connection between these mechanisms can be traced at the level of the hypothalamic-pituitary system. Humoral regulation arose earlier in phylogenesis. Later in the process of evolution it was supplemented with a highly specialized nervous system. The nervous system carries out its regulatory influences on organs and tissues with the help of nerve conductors that transmit nerve impulses.

It takes a fraction of a second to transmit a nerve signal. Therefore, the nervous system launches rapid adaptive reactions when the external or internal environment changes. Humoral regulation is the regulation of vital processes with the help of substances entering the internal environment of the body (blood, lymph, liquor). Humoral regulation ensures longer adaptive reactions. Factors of humoral regulation include hormones, electrolytes, mediators, kinins, prostaglandins, various metabolites, etc.

General physiology of the endocrine system

The highest form of humoral regulation is hormonal. The term “hormone” was first used in 1902 by Starling and Bayliss in relation to the substance they discovered produced in the duodenum, secretin. The term "hormone" is translated from Greek as "stimulating to action", although not all hormones have a stimulating effect.

Hormones are biologically highly active substances that are synthesized and released into the internal environment of the body by the endocrine glands, or endocrine glands, and have a regulatory effect on the functions of organs and systems of the body remote from the place of their secretion. An endocrine gland is an anatomical formation devoid of excretory ducts, the sole or main function of which is the internal secretion of hormones. The endocrine glands include the pituitary gland, pineal gland, thyroid gland, adrenal glands (medulla and cortex), and parathyroid glands.

Unlike internal secretion, external secretion is carried out by the exocrine glands through the excretory ducts into the external environment. In some organs both types of secretion are present simultaneously. The endocrine function is carried out by endocrine tissue, i.e. an accumulation of cells with an endocrine function in an organ that has functions not related to the production of hormones. Organs with a mixed type of secretion include the pancreas and gonads. The same endocrine gland can produce hormones that differ in their action. For example, the thyroid gland produces thyroxine and thyrocalcitonin. At the same time, the production of the same hormones can be carried out by different endocrine glands. For example, sex hormones are produced by both the gonads and the adrenal glands.

The production of biologically active substances is a function not only of the endocrine glands, but also of other traditionally non-endocrine organs: kidneys, gastrointestinal tract, heart. Not all substances produced by specific cells of these organs meet the classical criteria for the concept of “hormones”. Therefore, along with the term “hormone”, the concepts of hormone-like and biologically active substances (BAS), local hormones have recently also been used. For example, some of them are synthesized so close to their target organs that they can reach them by diffusion without entering the bloodstream. Cells that produce such substances are called paracrine. The difficulty of accurately defining the term “hormone” is especially clearly seen in the example of catecholamines - adrenaline and norepinephrine. When their production in the adrenal medulla is considered, they are usually called hormones; when we are talking about their formation and release by sympathetic endings, they are called mediators.

Regulatory hypothalamic hormones - a group of neuropeptides, including the recently discovered enkephalins and endorphins, act not only as hormones, but also perform a kind of mediator function. Some of the regulatory hypothalamic peptides are found not only in neurons of the brain, but also in special cells of other organs, such as the intestine: substance P, neurotensin, somatostatin, cholecystokinin, etc. The cells that produce these peptides form, according to modern concepts, a diffuse neuroendocrine system, consisting of cells scattered throughout different organs and tissues.

Cells of this system are characterized by a high amine content, the ability to take up amine precursors, and the presence of amine decarboxylase. Hence the name of the system after the first letters of the English words Amine Precursors Uptake and Decarboxylating system - APUD system - a system for capturing amine precursors and their decarboxylation. Therefore, it is legitimate to talk not only about the endocrine glands, but also about the endocrine system, which unites all the glands, tissues and cells of the body that secrete specific regulatory substances into the internal environment.

The chemical nature of hormones and biologically active substances is different. The duration of its biological action depends on the complexity of the structure of the hormone, for example, from fractions of a second for mediators and peptides to hours and days for steroid hormones and iodothyronines. Analysis of the chemical structure and physicochemical properties of hormones helps to understand the mechanisms of their action, develop methods for their determination in biological fluids and carry out their synthesis.

Classification of hormones and biologically active substances by chemical structure:

Amino acid derivatives: tyrosine derivatives: thyroxine, triiodothyronine, dopamine, adrenaline, norepinephrine; tryptophan derivatives: melatonin, serotonin; histidine derivatives: histamine.

Protein-peptide hormones: polypeptides: glucagon, corticotropin, melanotropin, vasopressin, oxytocin, peptide hormones of the stomach and intestines; simple proteins (proteins): insulin, somatotropin, prolactin, parathyroid hormone, calcitonin; complex proteins (glycoproteins): thyrotropin, follitropin, lutropin.

Steroid hormones: corticosteroids (aldosterone, cortisol, corticosterone); sex hormones: androgens (testosterone), estrogens and progesterone.

Fatty acid derivatives: arachidonic acid and its derivatives: prostaglandins, prostacyclins, thromboxanes, leukotrienes.

Despite the fact that hormones have different chemical structures, they share some common biological properties.

General properties of hormones:

Strict specificity (tropism) of physiological action.

High biological activity: hormones exert their physiological effects in extremely small doses.

Distant nature of action: target cells are usually located far from the site of hormone production.

Many hormones (steroids and amino acid derivatives) are not species specific.

Generalization of action.

Prolonged action.

Four main types of physiological effects on the body have been established: kinetic, or triggering, causing a certain activity of the executive organs; metabolic (metabolic changes); morphogenetic (differentiation of tissues and organs, effect on growth, stimulation of the formation process); corrective (change in intensity of functions of organs and tissues).

The hormonal effect is mediated by the following main stages: synthesis and entry into the blood, forms of transport, cellular mechanisms of hormone action. From the site of secretion, hormones are delivered to target organs by circulating fluids: blood, lymph. Hormones circulate in the blood in several forms: 1) in a free state; 2) in combination with specific blood plasma proteins; 3) in the form of a nonspecific complex with plasma proteins; 4) in an adsorbed state on the formed elements of blood. At rest, 80% is a complex with specific proteins. Biological activity is determined by the content of free forms of hormones. Bound forms of hormones are like a depot, a physiological reserve, from which hormones pass into the active free form as needed.

A prerequisite for the manifestation of the effects of a hormone is its interaction with receptors. Hormonal receptors are special cell proteins that are characterized by: 1) high affinity for the hormone; 2) high selectivity; 3) limited binding capacity; 4) specificity of receptor localization in tissues. Dozens of different types of receptors can be located on the same cell membrane. The number of functionally active receptors can change under various conditions and pathologies. For example, during pregnancy, M-cholinergic receptors disappear in the myometrium, and the number of oxytocin receptors increases. In some forms of diabetes mellitus, there is a functional failure of the insular apparatus, i.e. the level of insulin in the blood is high, but some of the insulin receptors are occupied by autoantibodies to these receptors. In 50% of cases, receptors are localized on the membranes of the target cell; 50% is inside the cell.

Mechanisms of action of hormones. There are two main mechanisms of action of hormones at the cellular level: the implementation of the effect from the outer surface of the cell membrane and the implementation of the effect after the penetration of the hormone into the cell.

In the first case, the receptors are located on the cell membrane. As a result of the interaction of the hormone with the receptor, the membrane enzyme adenylate cyclase is activated. This enzyme promotes the formation from adenosine triphosphate (ATP) of the most important intracellular mediator of hormonal effects - cyclic 3,5-adenosine monophosphate (cAMP). cAMP activates the cellular enzyme protein kinase, which realizes the action of the hormone. It has been established that hormone-dependent adenylate cyclase is a common enzyme that is acted upon by various hormones, while hormone receptors are multiple and specific for each hormone. Secondary messengers, in addition to cAMP, can be cyclic 3,5-guanosine monophosphate (cGMP), calcium ions, and inositol triphosphate. This is how peptide and protein hormones and tyrosine derivatives - catecholamines - act. A characteristic feature of the action of these hormones is the relative speed of the response, which is due to the activation of previous already synthesized enzymes and other proteins.

In the second case, receptors for the hormone are located in the cytoplasm of the cell. Hormones of this mechanism of action, due to their lipophilicity, easily penetrate the membrane into the target cell and bind to specific receptor proteins in its cytoplasm. The hormone-receptor complex enters the cell nucleus. In the nucleus, the complex disintegrates, and the hormone interacts with certain sections of nuclear DNA, resulting in the formation of a special messenger RNA. Messenger RNA leaves the nucleus and promotes the synthesis of protein or enzyme protein on ribosomes. This is how steroid hormones and tyrosine derivatives - thyroid hormones - act. Their action is characterized by a deep and long-term restructuring of cellular metabolism.

Inactivation of hormones occurs in effector organs, mainly the liver, where hormones undergo various chemical changes by binding to glucuronic or sulfuric acid or as a result of the action of enzymes. Partially the hormones are excreted unchanged in the urine. The action of some hormones can be blocked due to the secretion of hormones that have an antagonistic effect.

Hormones perform the following important functions in the body:

Regulation of growth, development and differentiation of tissues and organs, which determines physical, sexual and mental development.

Ensuring the body's adaptation to changing living conditions.

Ensuring the maintenance of homeostasis.

Functional classification of hormones:

Effector hormones are hormones that directly affect the target organ.

Triple hormones are hormones whose main function is to regulate the synthesis and release of effector hormones. Produced by the adenohypophysis.

Releasing hormones are hormones that regulate the synthesis and secretion of adenohypophysis hormones, mainly triple ones. They are secreted by nerve cells of the hypothalamus.

Types of hormone interactions. Each hormone does not work alone. Therefore, it is necessary to take into account the possible results of their interaction.

Synergism is the unidirectional action of two or more hormones. For example, adrenaline and glucagon activate the breakdown of liver glycogen into glucose and cause an increase in blood sugar levels.

Antagonism is always relative. For example, insulin and epinephrine have opposite effects on blood glucose levels. Insulin causes hypoglycemia, adrenaline causes hyperglycemia. The biological significance of these effects boils down to one thing - improving the carbohydrate nutrition of tissues.

The permissive effect of hormones is that the hormone, without causing a physiological effect, creates the conditions for a cell or organ to respond to the action of another hormone. For example, glucocorticoids, without affecting vascular muscle tone and the breakdown of liver glycogen, create conditions under which even small concentrations of adrenaline increase blood pressure and cause hyperglycemia as a result of glycogenolysis in the liver.

Regulation of the functions of the endocrine glands

Regulation of the activity of the endocrine glands is carried out by nervous and humoral factors. The neuroendocrine zones of the hypothalamus, pineal gland, adrenal medulla and other areas of chromaffin tissue are regulated directly by nervous mechanisms. In most cases, the nerve fibers approaching the endocrine glands regulate not the secretory cells, but the tone of the blood vessels, on which the blood supply and functional activity of the glands depend. The main role in the physiological mechanisms of regulation is played by neurohormonal and hormonal mechanisms, as well as direct effects on the endocrine glands of those substances whose concentration is regulated by this hormone.

The regulatory influence of the central nervous system on the activity of the endocrine glands is carried out through the hypothalamus. The hypothalamus receives signals from the external and internal environment through the afferent pathways of the brain. Neurosecretory cells of the hypothalamus transform afferent nerve stimuli into humoral factors, producing releasing hormones. Releasing hormones selectively regulate the functions of adenohypophysis cells. Among the releasing hormones, there are liberins - stimulators of the synthesis and release of adenohypophysis hormones and statins - secretion inhibitors. They are called the corresponding tropic hormones: thyrotropin-releasing hormone, corticoliberin, somatoliberin, etc. In turn, tropic hormones of the adenohypophysis regulate the activity of a number of other peripheral endocrine glands (adrenal cortex, thyroid gland, gonads). These are the so-called direct downward regulatory connections.

In addition to them, within these systems there are also reverse ascending self-regulating connections. Feedback can come from both the peripheral gland and the pituitary gland. Depending on the direction of physiological action, feedback can be negative and positive. Negative connections self-limit the operation of the system. Positive connections self-start it. Thus, low concentrations of thyroxine through the blood increase the production of thyroid-stimulating hormone by the pituitary gland and thyroid-releasing hormone by the hypothalamus. The hypothalamus is much more sensitive than the pituitary gland to hormonal signals coming from the peripheral endocrine glands. Thanks to the feedback mechanism, a balance is established in the synthesis of hormones, responding to a decrease or increase in the concentration of hormones of the endocrine glands.

Some endocrine glands, such as the pancreas and parathyroid glands, are not influenced by pituitary hormones. The activity of these glands depends on the concentration of those substances whose levels are regulated by these hormones. Thus, the level of parathyroid hormone of the parathyroid glands and calcitonin of the thyroid gland is determined by the concentration of calcium ions in the blood. Glucose regulates the production of insulin and glucagon by the pancreas. In addition, the functioning of these glands is carried out due to the influence of the level of antagonist hormones.

Pituitary

The pituitary gland plays a special role in the system of endocrine glands. With the help of its hormones, it regulates the activity of other endocrine glands.

The pituitary gland consists of the anterior (adenohypophysis), intermediate and posterior (neurohypophysis) lobes. The intermediate lobe is practically absent in humans.

Hormones of the anterior pituitary gland

The following hormones are produced in the adenohypophysis: adrenocorticotropic hormone (ACTH), or corticotropin; thyroid stimulating hormone (TSH), or thyrotropin, gonadotropic: follicle stimulating hormone (FSH), or follitropin, and luteinizing hormone (LH), or lutropin, somatotropic hormone (GH), or growth hormone, or somatotropin, prolactin. The first 4 hormones regulate the functions of the so-called peripheral endocrine glands. Somatotropin and prolactin themselves act on target tissues.

Adrenocorticotropic hormone (ACTH), or corticotropin, has a stimulating effect on the adrenal cortex. To a greater extent, its influence is expressed on the zona fasciculata, which leads to an increase in the formation of glucocorticoids, and to a lesser extent on the glomerular and reticular zones, therefore it does not have a significant effect on the production of mineralocorticoids and sex hormones. Due to increased protein synthesis (cAMP-dependent activation), hyperplasia of the adrenal cortex occurs. ACTH enhances cholesterol synthesis and the rate of formation of pregnenolone from cholesterol. Extra-adrenal effects of ACTH include stimulation of lipolysis (mobilizes fats from fat depots and promotes fat oxidation), increased secretion of insulin and somatotropin, accumulation of glycogen in muscle cells, hypoglycemia, which is associated with increased secretion of insulin, increased pigmentation due to the effect on melanophore pigment cells .

ACTH production is subject to daily periodicity, which is associated with the rhythmicity of corticoliberin release. The maximum concentrations of ACTH are observed in the morning at 6 - 8 o'clock, the minimum - from 18 to 23 o'clock. ACTH production is regulated by hypothalamic corticoliberin. The secretion of ACTH increases under stress, as well as under the influence of factors that cause stressful conditions: cold, pain, physical activity, emotions. Hypoglycemia increases ACTH production. Inhibition of ACTH production occurs under the influence of glucocorticoids themselves via a feedback mechanism.

Excess ACTH leads to hypercortisolism, i.e. increased production of corticosteroids, mainly glucocorticoids. This disease develops with pituitary adenoma and is called Itsenko-Cushing's disease. Its main manifestations are: hypertension, obesity, which is local in nature (face and torso), hyperglycemia, decreased immune defense of the body.

Lack of the hormone leads to a decrease in the production of glucocorticoids, which is manifested by metabolic disorders and a decrease in the body’s resistance to various environmental influences.

Thyroid-stimulating hormone (TSH), or thyrotropin, activates the function of the thyroid gland, causes hyperplasia of its glandular tissue, and stimulates the production of thyroxine and triiodothyronine. The formation of thyrotropin is stimulated by thyrotropin-releasing hormone in the hypothalamus and inhibited by somatostatin. The secretion of thyroid hormones and thyrotropin is regulated by iodine-containing thyroid hormones via a feedback mechanism. The secretion of thyrotropin also increases when the body cools, which leads to increased production of thyroid hormones and increased heat. Glucocorticoids inhibit the production of thyrotropin. The secretion of thyrotropin is also inhibited during injury, pain, and anesthesia.

Excess thyrotropin is manifested by hyperfunction of the thyroid gland, the clinical picture of thyrotoxicosis.

Follicle-stimulating hormone (FSH), or follitropin, causes the ovarian follicles to grow and mature and prepare them for ovulation. In men, under the influence of FSH, sperm formation occurs.

Luteinizing hormone (LH), or lutropin, promotes rupture of the membrane of a mature follicle, i.e. ovulation and the formation of the corpus luteum. LH stimulates the formation of female sex hormones - estrogens. In men, this hormone promotes the formation of male sex hormones - androgens.

The secretion of FSH and drugs is regulated by GnRH of the hypothalamus. The formation of GnRH, FSH and LH depends on the level of estrogens and androgens and is regulated by a feedback mechanism. The adenohypophysis hormone prolactin inhibits the production of gonadotropic hormones. Glucocorticoids have an inhibitory effect on the release of LH.

Somatotropic hormone (GH), or somatotropin, or growth hormone, takes part in the regulation of the processes of growth and physical development. Stimulation of growth processes is due to the ability of somatotropin to enhance protein formation in the body, increase RNA synthesis, and enhance the transport of amino acids from the blood to cells. The effect of the hormone is most pronounced on bone and cartilage tissue. The action of somatotropin occurs through “somatomedins”, which are formed in the liver under the influence of somatotropin. It was found that in pygmies, against the background of normal somatotropin levels, somatomedin C is not formed, which, according to researchers, is the reason for their short stature. Somatotropin affects carbohydrate metabolism, producing an insulin-like effect. The hormone enhances the mobilization of fat from the depot and its use in energy metabolism.

The production of somatotropin is regulated by somatoliberin and somatostatin of the hypothalamus. A decrease in the content of glucose and fatty acids, an excess of amino acids in the blood plasma also lead to an increase in the secretion of somatotropin. Vasopressin and endorphin stimulate the production of somatotropin.

If hyperfunction of the anterior lobe of the pituitary gland manifests itself in childhood, this leads to increased proportional growth in length - gigantism. If hyperfunction occurs in an adult, when the growth of the body as a whole has already been completed, there is an increase in only those parts of the body that are still capable of growing. These are fingers and toes, hands and feet, nose and lower jaw, tongue, organs of the chest and abdominal cavities. This disease is called acromegaly. The cause is benign pituitary tumors. Hypofunction of the anterior lobe of the pituitary gland in childhood is expressed in growth retardation - dwarfism ("pituitary dwarfism"). Mental development is not impaired.

Somatotropin is species specific.

Prolactin stimulates the growth of mammary glands and promotes milk formation. The hormone stimulates the synthesis of protein - lactalbumin, fats and carbohydrates in milk. Prolactin also stimulates the formation of the corpus luteum and its production of progesterone. Affects the body's water-salt metabolism, retaining water and sodium in the body, enhances the effects of aldosterone and vasopressin, and increases the formation of fat from carbohydrates.

The formation of prolactin is regulated by prolactoliberin and prolactostatin in the hypothalamus. It has also been established that stimulation of prolactin secretion is also caused by other peptides secreted by the hypothalamus: thyrotropin-releasing hormone, vasoactive intestinal polypeptide (VIP), angiotensin II, probably the endogenous opioid peptide B-endorphin. The secretion of prolactin increases after childbirth and is reflexively stimulated during breastfeeding. Estrogens stimulate the synthesis and secretion of prolactin. Dopamine of the hypothalamus inhibits the production of prolactin, which probably also inhibits the hypothalamic cells that secrete GnRH, which leads to menstrual irregularities - lactogenic amenorrhea.

Excess prolactin is observed with benign pituitary adenoma (hyperprolactinemic amenorrhea), with meningitis, encephalitis, brain injury, excess estrogen, and with the use of certain contraceptives. Its manifestations include milk production in non-breastfeeding women (galactorrhea) and amenorrhea. Drugs that block dopamine receptors (especially often with psychotropic effects) also lead to increased secretion of prolactin, which can result in galactorrhea and amenorrhea.

Posterior pituitary hormones

These hormones are produced in the hypothalamus. They accumulate in the neurohypophysis. In the cells of the supraoptic and paraventricular nuclei of the hypothalamus, oxytocin and antidiuretic hormone are synthesized. Synthesized hormones are transported through axonal transport with the help of the neurophysin transporter protein along the hypothalamic-pituitary tract to the posterior lobe of the pituitary gland. Here, hormones are deposited and subsequently released into the blood.

Antidiuretic. hormone (ADH), or vasopressin, performs 2 main functions in the body. The first function is its antidiuretic effect, which is expressed in stimulating the reabsorption of water in the distal nephron. This action is carried out due to the interaction of the hormone with vasopressin receptors of type V-2, which leads to increased permeability of the wall of the tubules and collecting ducts for water, its reabsorption and concentration of urine. Activation of hyaluronidase also occurs in tubular cells, which leads to increased depolymerization of hyaluronic acid, resulting in increased water reabsorption and an increase in the volume of circulating fluid.

In large (pharmacological) doses, ADH constricts arterioles, resulting in increased blood pressure. Therefore, it is also called vasopressin. Under normal conditions, at its physiological concentrations in the blood, this effect is not significant. However, with blood loss and painful shock, an increase in ADH release occurs. Vasoconstriction in these cases may have adaptive significance.

The formation of ADH increases with an increase in blood osmotic pressure, a decrease in the volume of extracellular and intracellular fluid, a decrease in blood pressure, and with activation of the renin-angiotensin system and the sympathetic nervous system.

If the formation of ADH is insufficient, diabetes insipidus, or diabetes insipidus, develops, which is manifested by the release of large amounts of urine (up to 25 liters per day) of low density, increased thirst. The causes of diabetes insipidus can be acute and chronic infections that affect the hypothalamus (influenza, measles, malaria), traumatic brain injury, or a tumor of the hypothalamus.

Excessive secretion of ADH, on the contrary, leads to water retention in the body.

Oxytocin selectively acts on the smooth muscles of the uterus, causing its contractions during childbirth. There are special oxytocin receptors on the surface membrane of cells. During pregnancy, oxytocin does not increase the contractile activity of the uterus, but before childbirth, under the influence of high concentrations of estrogen, the sensitivity of the uterus to oxytocin sharply increases. Oxytocin is involved in the process of lactation. By enhancing the contractions of myoepithelial cells in the mammary glands, it promotes milk secretion. An increase in the secretion of oxytocin occurs under the influence of impulses from the receptors of the cervix, as well as mechanoreceptors of the nipples of the mammary gland during breastfeeding. Estrogens increase the secretion of oxytocin. The functions of oxytocin in the male body have not been sufficiently studied. It is believed to be an antagonist of ADH.

Lack of oxytocin production causes weakness of labor.

Thyroid. Parathyroid glands

Thyroid

The thyroid gland consists of two lobes connected by an isthmus and located in the neck on either side of the trachea below the thyroid cartilage. It has a lobular structure. The gland tissue consists of follicles filled with colloid, which contains the iodine-containing hormones thyroxine (tetraiodothyronine) and triiodothyronine bound to the protein thyroglobulin. In the interfollicular space there are parafollicular cells that produce the hormone thyrocalcitonin. The content of thyroxine in the blood is higher than triiodothyronine. However, the activity of triiodothyronine is higher than that of thyroxine. These hormones are formed from the amino acid tyrosine by iodization. Inactivation occurs in the liver through the formation of paired compounds with glucuronic acid.

Iodine-containing hormones perform the following functions in the body: 1) strengthening all types of metabolism (protein, lipid, carbohydrate), increasing basal metabolism and enhancing energy production in the body; 2) influence on growth processes, physical and mental development; 3) increase in heart rate; 4) stimulation of the digestive tract: increased appetite, increased intestinal motility, increased secretion of digestive juices; 5) increase in body temperature due to increased heat production; 6) increased excitability of the sympathetic nervous system.

The secretion of thyroid hormones is regulated by thyroid-stimulating hormone of the adenohypophysis, thyroid-releasing hormone of the hypothalamus, and iodine content in the blood. With a lack of iodine in the blood, as well as iodine-containing hormones, the production of thyrotropin-releasing hormone increases through a positive feedback mechanism, which stimulates the synthesis of thyroid-stimulating hormone, which, in turn, leads to an increase in the production of thyroid hormones. With an excess amount of iodine in the blood and thyroid hormones A negative feedback mechanism operates: Excitation of the sympathetic part of the autonomic nervous system stimulates the hormone-producing function of the thyroid gland, and excitation of the parasympathetic part inhibits it.

Disorders of the thyroid gland are manifested by its hypofunction and hyperfunction. If insufficiency of function develops in childhood, this leads to growth retardation, disturbance of body proportions, sexual and mental development. This pathological condition is called cretinism. In adults, hypofunction of the thyroid gland leads to the development of a pathological condition - myxedema. With this disease, inhibition of neuropsychic activity is observed, which manifests itself in lethargy, drowsiness, apathy, decreased intelligence, decreased excitability of the sympathetic part of the autonomic nervous system, impaired sexual function, inhibition of all types of metabolism and a decrease in basal metabolism. Such patients have increased body weight for due to an increase in the amount of tissue fluid and puffiness of the face is noted. Hence the name of this disease: myxedema - mucous swelling

Hypofunction of the thyroid gland can develop in people living in areas where there is a lack of iodine in the water and soil. This is the so-called endemic goiter. In this disease, the thyroid gland is enlarged (goiter), the number of follicles increases, however, due to a lack of iodine, few o6 hormones are produced, which leads to corresponding disorders in the body, manifested in the form of hypothyroidism.

With hyperfunction of the thyroid gland, the disease thyrotoxicosis develops (diffuse toxic goiter, Basedow's disease, Graves' disease). Characteristic signs of this disease are enlargement of the thyroid gland (goiter), exophthalmos, tachycardia, increased metabolism, especially the basal one, loss of body weight, increased appetite, disturbance of the body's thermal balance, increased excitability and irritability.

Calcitonin, or thyrocalcitonin, together with parathyroid hormone of the parathyroid glands, is involved in the regulation of calcium metabolism. Under its influence, the level of calcium in the blood decreases (hypocalcemia). This occurs as a result of the hormone’s action on bone tissue, where it activates the function of osteoblasts and enhances mineralization processes. The function of osteoclasts, which destroy bone tissue, on the contrary, is inhibited. In the kidneys and intestines, calcitonin inhibits the reabsorption of calcium and enhances the reabsorption of phosphates. The production of thyrocalcitonin is regulated by the level of calcium in the blood plasma according to the feedback type. When calcium levels decrease, the production of thyrocalcitonin is inhibited, and vice versa.

Parathyroid glands

A person has 2 pairs of parathyroid glands, located on the back surface or embedded inside the thyroid gland. The chief, or oxyphilic, cells of these glands produce parathyroid hormone, or parathyrin, or parathyroid hormone (PTH). Parathyroid hormone regulates calcium metabolism in the body and maintains its level in the blood. In bone tissue, parathyroid hormone enhances the function of osteoclasts, which leads to bone demineralization and increased calcium levels in the blood plasma (hypercalcemia). In the kidneys, parathyroid hormone enhances calcium reabsorption. In the intestine, an increase in calcium reabsorption occurs due to the stimulating effect of parathyroid hormone on the synthesis of calcitriol, the active metabolite of vitamin D3. Vitamin D3 is formed in an inactive state in the skin under the influence of ultraviolet radiation. Under the influence of parathyroid hormone, it is activated in the liver and kidneys. Calcitriol increases the formation of calcium-binding protein in the intestinal wall, which promotes the reabsorption of calcium. Influencing calcium metabolism, parathyroid hormone simultaneously affects phosphorus metabolism in the body: it inhibits the reabsorption of phosphates and increases their excretion in the urine (phosphaturia).

The activity of the parathyroid glands is determined by the calcium content in the blood plasma. If the concentration of calcium in the blood increases, this leads to a decrease in the secretion of parathyroid hormone. A decrease in calcium levels in the blood causes increased production of parathyroid hormone.

Removal of the parathyroid glands in animals or their hypofunction in humans leads to increased neuromuscular excitability, which is manifested by fibrillary twitching of single muscles, turning into spastic contractions of muscle groups, mainly the limbs, face and back of the head. The animal dies from tetanic convulsions.

Hyperfunction of the parathyroid glands leads to demineralization of bone tissue and the development of osteoporosis. Hypercalcemia increases the tendency to stone formation in the kidneys, contributes to the development of disturbances in the electrical activity of the heart, and the occurrence of ulcers in the gastrointestinal tract as a result of increased amounts of gastrin and HCl in the stomach, the formation of which is stimulated by calcium ions.

Adrenal glands

The adrenal glands are paired glands. It is an endocrine organ that is of vital importance. The adrenal glands have two layers - the cortex and the medulla. The cortical layer is of mesodermal origin, the medulla develops from the rudiment of the sympathetic ganglion.

Adrenal cortex hormones

In the adrenal cortex there are 3 zones: the outer - glomerular, the middle - fasciculata and the inner - reticularis. In the zona glomerulosa, mainly mineralocorticoids are produced, in the zona fasciculata - glucocorticoids, in the reticularis - sex hormones (mainly androgens). According to their chemical structure, adrenal hormones are steroids. The mechanism of action of all steroid hormones is to directly influence the genetic apparatus of the cell nucleus, stimulate the synthesis of the corresponding RNA, activate the synthesis of cation transporting proteins and enzymes, and also increase the permeability of membranes to amino acids.

Mineralocorticoids. This group includes aldosterone, deoxycorticosterone, 18-hydroxycorticosterone, 18-oxydeoxycorticosterone. These hormones are involved in the regulation of mineral metabolism. The main representative of mineralocorticoids is aldosterone. Aldosterone enhances the reabsorption of sodium and chlorine ions in the distal renal tubules and reduces the reabsorption of potassium ions. As a result, urinary sodium excretion decreases and potassium excretion increases. As sodium is reabsorbed, water reabsorption also passively increases. Due to water retention in the body, the volume of circulating blood increases, blood pressure increases, and diuresis decreases. Aldosterone has a similar effect on the exchange of sodium and potassium in the salivary and sweat glands.

Aldosterone promotes the development of the inflammatory response. Its anti-inflammatory effect is associated with increased exudation of fluid from the lumen of blood vessels into the tissue and tissue swelling. With increased production of aldosterone, the secretion of hydrogen ions and ammonium in the renal tubules also increases, which can lead to a change in the acid-base state - alkalosis.

There are several mechanisms involved in the regulation of aldosterone levels in the blood, the main one being the renin-angiotensin-aldosterone system. To a small extent, aldosterone production is stimulated by ACTH of the adenohypophysis. Hyponatremia or hyperkalemia stimulates the production of aldosterone through a feedback mechanism. Atrial natriuretic hormone is an aldosterone antagonist.

Glucocorticoids. Glucocorticoid hormones include cortisol, cortisone, corticosterone, 11-deoxycortisol, 11-dehydrocorticosterone. In humans, the most important glucocorticoid is cortisol. These hormones influence the metabolism of carbohydrates, proteins and fats:

Glucocorticoids cause an increase in plasma glucose (hyperglycemia). This effect is due to the stimulation of gluconeogenesis processes in the liver, i.e. formation of glucose from amino acids and fatty acids. Glucocorticoids inhibit the activity of the hexokinase enzyme, which leads to a decrease in glucose utilization by tissues. Glucocorticoids are insulin antagonists in the regulation of carbohydrate metabolism.

Glucocorticoids have a catabolic effect on protein metabolism. At the same time, they also have a pronounced anti-anabolic effect, which is manifested by a decrease in the synthesis of especially muscle proteins, since Glucocorticoids inhibit the transport of amino acids from the blood plasma to muscle cells. As a result, muscle mass decreases, osteoporosis may develop, and the rate of wound healing decreases.

The effect of glucocorticoids on fat metabolism is to activate lipolysis, which leads to an increase in the concentration of fatty acids in the blood plasma.

Glucocorticoids inhibit all components of the inflammatory reaction: they reduce capillary permeability, inhibit exudation and reduce tissue swelling, stabilize lysosome membranes, which prevents the release of proteolytic enzymes that contribute to the development of the inflammatory reaction, and inhibit phagocytosis at the site of inflammation. Glucocorticoids reduce fever. This action is associated with a decrease in the release of interleukin-1 from leukocytes, which stimulates the heat production center in the hypothalamus.

Glucocorticoids have an antiallergic effect. This action is due to the effects underlying the anti-inflammatory effect: inhibition of the formation of factors that enhance the allergic reaction, reduction of exudation, stabilization of lysosomes. An increase in the content of glucocorticoids in the blood leads to a decrease in the number of eosinophils, the concentration of which is usually increased during allergic reactions.

Glucocorticoids inhibit both cellular and humoral immunity. They reduce the production of T and B lymphocytes, reduce the formation of antibodies, and reduce immunological surveillance. With long-term use of glucocorticoids, involution of the thymus and lymphoid tissue may occur. Weakening of the body's protective immune reactions is a serious side effect of long-term treatment with glucocorticoids, as the likelihood of a secondary infection increases. In addition, the danger of developing a tumor process increases due to depression of immunological surveillance. On the other hand, these effects of glucocorticoids allow us to consider them as active immunosuppressants.

Glucocorticoids increase the sensitivity of vascular smooth muscle to catecholamines, which can lead to an increase in blood pressure. This is also facilitated by their slight mineralocorticoid effect: sodium and water retention in the body.

Glucocorticoids stimulate the secretion of hydrochloric acid.

The production of glucocorticoids by the adrenal cortex is stimulated by ACTH of the adenohypophysis. Excessive levels of glucocorticoids in the blood lead to inhibition of the synthesis of ACTH and corticoliberin by the hypothalamus. Thus, the hypothalamus, adenohypophysis and adrenal cortex are functionally united and therefore form a single hypothalamic-pituitary-adrenal system. In acute stressful situations, the level of glucocorticoids in the blood quickly increases. Due to their metabolic effects, they quickly provide the body with energy material.

Hypofunction of the adrenal cortex is manifested by a decrease in the content of corticoid hormones and is called Addison's (bronze) disease. The main symptoms of this disease are: adynamia, decreased circulating blood volume, arterial hypotension, hypoglycemia, increased skin pigmentation, dizziness, vague abdominal pain, diarrhea.

With adrenal tumors, hyperfunction of the adrenal cortex with excessive production of glucocorticoids may develop. This is the so-called primary hypercorticism, or Itsenko-Cushing syndrome. The clinical manifestations of this syndrome are the same as with Itsenko-Cushing's disease.

Sex hormones play a certain role only in childhood, when the intrasecretory function of the gonads is still poorly developed. Sex hormones from the adrenal cortex contribute to the development of secondary sexual characteristics. They also stimulate protein synthesis in the body. ACTH stimulates the synthesis and secretion of androgens. With excessive production of sex hormones by the adrenal cortex, adrenogenital syndrome develops. If there is an excessive formation of hormones of the same sex, then the process of sexual development is accelerated, if of the opposite sex, then secondary sexual characteristics characteristic of the other sex appear.

Hormones of the adrenal medulla

The adrenal medulla produces catecholamines; adrenaline and norepinephrine. Adrenaline accounts for about 80%, and norepinephrine accounts for about 20% of hormonal secretion. The secretion of adrenaline and norepinephrine is carried out by chromaffin cells from the amino acid tyrosine (tyrosine-DOPA-dopamine-norepinephrine-adrenaline). Inactivation is carried out by monoamine oxidase and catechol-methyltransferase.

The physiological effects of epinephrine and norepinephrine are similar to the activation of the sympathetic nervous system, but the hormonal effect is longer lasting. At the same time, the production of these hormones increases when the sympathetic part of the autonomic nervous system is excited. Adrenaline stimulates the activity of the heart, constricts blood vessels, except for the coronary vessels, the vessels of the lungs, the brain, and working muscles, on which it has a vasodilator effect. Adrenaline relaxes the muscles of the bronchi, inhibits peristalsis and intestinal secretion and increases the tone of the sphincters, dilates the pupil, reduces sweating, and enhances the processes of catabolism and energy formation. Adrenaline expression affects carbohydrate metabolism, increasing the breakdown of glycogen in the liver and muscles, resulting in an increase in glucose levels in the blood plasma. Adrenaline activates lipolysis. Catecholamines are involved in the activation of thermogenesis.

The actions of adrenaline and norepinephrine are mediated by their interaction with a and b-adrenergic receptors, which, in turn, are pharmacologically divided into a1-, a2-, b1- and b2-receptors. Adrenaline has a greater affinity for b-adrenergic receptors, norepinephrine - for a-adrenergic receptors. In clinical practice, substances that selectively excite or block these receptors are widely used.

Excessive secretion of catecholamines is observed in tumors of the chromaffin substance of the adrenal glands - pheochromocytoma. Its main manifestations include: paroxysmal increases in blood pressure, attacks of tachycardia, shortness of breath.

When the body is exposed to emergency or pathological factors of various nature (trauma, hypoxia, cooling, bacterial intoxication, etc.), the same type of nonspecific changes occur in the body, aimed at increasing its nonspecific resistance, called the general adaptation syndrome (G. Selye) . The pituitary-adrenal system plays a major role in the development of adaptation syndrome.

Pancreas

The pancreas is a mixed-function gland. Endocrine function is carried out through the production of hormones by the pancreatic islets (islets of Langerhans). The islets are located predominantly in the caudal part of the gland, and a small number of them are located in the head section. There are several types of cells in the islets: a, b, d, G and PP. a-cells produce glucagon, b-cells produce insulin, d-cells synthesize somatostatin, which inhibits the secretion of insulin and glucagon. G cells produce gastrin; PP cells produce a small amount of pancreatic polypeptide, which is an antagonist of cholecystokinin. The bulk are made up of b-cells that produce insulin.

Insulin affects all types of metabolism, but primarily carbohydrate metabolism. Under the influence of insulin, a decrease in the concentration of glucose in the blood plasma occurs (hypoglycemia). This is because insulin promotes the conversion of glucose into glycogen in the liver and muscles (glycogenesis). It activates enzymes involved in the conversion of glucose into liver glycogen and inhibits enzymes that break down glycogen. Insulin also increases the permeability of the cell membrane to glucose, which enhances its utilization. In addition, insulin inhibits the activity of enzymes that provide gluconeogenesis, thereby inhibiting the formation of glucose from amino acids. Insulin stimulates protein synthesis from amino acids and reduces protein catabolism. Insulin regulates fat metabolism, enhancing the processes of lipogenesis: it promotes the formation of fatty acids from carbohydrate metabolism products, inhibits the mobilization of fat from adipose tissue and promotes the deposition of fat in fat depots.

The formation of insulin is regulated by the level of glucose in the blood plasma. Hyperglycemia increases insulin production, while hypoglycemia reduces the formation and flow of the hormone into the blood. Some gastrointestinal hormones, such as gastric inhibitory peptide, cholecystokinin, secretin, increase insulin output. The vagus nerve and acetylcholine enhance insulin production, while the sympathetic nerves and norepinephrine suppress insulin secretion.

Insulin antagonists by the nature of their effect on carbohydrate metabolism are glucagon, ACTH, somatotropin, glucocorticoids, adrenaline, thyroxine. The administration of these hormones causes hyperglycemia.

Insufficient secretion of insulin leads to a disease called diabetes mellitus. The main symptoms of this disease are hylerglycemia, glucosuria, polyuria, and polydipsia. In patients with diabetes, not only carbohydrate, but also protein and fat metabolism is disrupted. Lipolysis increases with the formation of a large amount of unbound fatty acids, and the synthesis of ketone bodies occurs. Protein catabolism leads to weight loss. Intensive formation of acidic products of fat breakdown and deamination of amino acids in the liver can cause a shift in the blood reaction towards acidosis and the development of hyperglycemic diabetic coma, which is manifested by loss of consciousness, respiratory and circulatory disorders.

Excessive insulin in the blood (for example, with an islet cell tumor or with an overdose of exogenous insulin) causes hypoglycemia and can lead to disruption of the energy supply to the brain and loss of consciousness (hypoglycemic coma).

a-Cells of the islets of Langerhans synthesize glucagon, which is an insulin antagonist. Under the influence of glucagon, glycogen breaks down in the liver to glucose. As a result, the glucose level in the blood increases. Glucagon promotes the mobilization of fat from fat depots. Glucagon secretion also depends on the concentration of glucose in the blood. Hyperglycemia inhibits the formation of glucagon; hypoglycemia, on the contrary, increases it.

Sex glands

Sex glands, or gonads - testes (testes) in men and ovaries in women are among the glands with mixed secretion. External secretion is associated with the formation of male and female germ cells - sperm and eggs. The intrasecretory function consists of the secretion of male and female sex hormones and their release into the blood. Both the testes and ovaries synthesize both male and female sex hormones, but androgens predominate in men, and estrogens in women. Sex hormones promote embryonic differentiation, the subsequent development of genital organs and the appearance of secondary sexual characteristics, and determine puberty and human behavior. In the female body, sex hormones regulate the ovarian-menstrual cycle, and also ensure the normal course of pregnancy and the preparation of the mammary glands for milk secretion.

Male sex hormones (androgens)

The interstitial cells of the testicles (Leydig cells) produce male sex hormones. They are also produced in small quantities in the zona reticularis of the adrenal cortex in men and women and in the outer layer of the ovaries in women. All sex hormones are steroids and are synthesized from one precursor - cholesterol. The most important of the androgens is testosterone. Testosterone is destroyed in the liver, and its metabolites are excreted in the urine in the form of 17-ketosteroids. The concentration of testosterone in blood plasma has daily fluctuations. The maximum level is observed at 7-9 am, the minimum - from 24 to 3 am.

Testosterone is involved in the sexual differentiation of the gonad and ensures the development of primary (growth of the penis and testicles) and secondary (male hair type, low voice, characteristic body structure, mental and behavioral characteristics) sexual characteristics, and the appearance of sexual reflexes. The hormone is also involved in the maturation of male germ cells - sperm, which are formed in the spermatogenic epithelial cells of the seminiferous tubules. Testosterone has a pronounced anabolic effect, i.e. increases protein synthesis, especially in muscles, which leads to an increase in muscle mass, accelerating the processes of growth and physical development. By accelerating the formation of the protein matrix of the bone, as well as the deposition of calcium salts in it, the hormone ensures bone growth, thickness and strength. By promoting ossification of epiphyseal cartilage, sex hormones practically stop bone growth. Testosterone reduces body fat. The hormone stimulates erythropoiesis, which explains the greater number of red blood cells in men than in women. Testosterone influences the activity of the central nervous system, determining sexual behavior and typical psychophysiological traits of men.

Testosterone production is regulated by luteinizing hormone of the adenohypophysis via a feedback mechanism. An increased level of testosterone in the blood inhibits the production of lutropin, while a decreased level accelerates it. Sperm maturation occurs under the influence of FSH. Sertoli cells, along with their participation in spermatogenesis, synthesize and secrete the hormone inhibin into the lumen of the seminiferous tubules, which inhibits the production of FSH.

Insufficient production of male sex hormones may be associated with the development of a pathological process in the testicular parenchyma (primary hypogonadism) and due to hypothalamic-pituitary insufficiency (secondary hypogonadism). There are congenital and acquired primary hypogonadism. The causes of congenital are dysgenesis of the seminiferous tubules, dysgenesis or testicular aplasia. Acquired testicular dysfunction occurs as a result of surgical castration, trauma, tuberculosis, syphilis, gonorrhea, complications of orchitis, for example, mumps. Manifestations of the disease depend on the age at which testicular damage occurred.

With congenital underdevelopment of the testicles or if they are damaged before puberty, eunuchoidism occurs. The main symptoms of this disease are underdevelopment of the internal and external genital organs, as well as secondary sexual characteristics. Such men have a small body size and long limbs, increased fat deposition on the chest, thighs and lower abdomen, poor muscle development, high pitched voice, enlarged mammary glands (gynecomastia), lack of libido, and infertility. With a disease that develops in postpuberty, underdevelopment of the genital organs is less pronounced. Libido is often preserved. There are no skeletal disproportions. Symptoms of demasculinization are observed: decreased hair growth, decreased muscle strength, female-type obesity, weakened potency up to impotence, infertility. Increased production of male sex hormones in childhood leads to premature puberty. Excess testosterone in post-puberty causes hypersexuality and increased hair growth.

Female sex hormones

These hormones are produced in the female gonads - the ovaries, during pregnancy - in the placenta, and also in small quantities by the Sertoli cells of the testes in men. Estrogen synthesis occurs in the ovarian follicles, and the corpus luteum of the ovary produces progesterone.

Estrogens include estrone, estradiol and estriol. Estradiol has the greatest physiological activity. Estrogens stimulate the development of primary and secondary female sexual characteristics. Under their influence, the ovaries, uterus, fallopian tubes, vagina and external genitalia grow, and proliferation processes in the endometrium intensify. Estrogens stimulate the development and growth of mammary glands. In addition, estrogens affect the development of the bone skeleton, accelerating its maturation. Due to their effect on epiphyseal cartilages, they inhibit the growth of bones in length. Estrogens have a pronounced anabolic effect, enhance the formation of fat and its distribution, typical of the female figure, and also promote female-type hair growth. Estrogens retain nitrogen, water, and salts. Under the influence of these hormones, the emotional and mental state of women changes. During pregnancy, estrogens promote the growth of uterine muscle tissue, effective uteroplacental circulation, and, together with progesterone and prolactin, the development of the mammary glands.

During ovulation, the hormone progesterone is produced in the corpus luteum of the ovary, which develops at the site of the burst follicle. The main function of progesterone is to prepare the endometrium for implantation of a fertilized egg and ensure the normal course of pregnancy. If fertilization does not occur, the corpus luteum degenerates. During pregnancy, progesterone, together with estrogens, causes morphological changes in the uterus and mammary glands, enhancing the processes of proliferation and secretory activity. As a result, the concentrations of lipids and glycogen necessary for the development of the embryo increase in the secretion of the endometrial glands. The hormone inhibits the ovulation process. In non-pregnant women, progesterone is involved in the regulation of the menstrual cycle. Progesterone increases basal metabolism and increases basal body temperature, which is used in practice to determine the time of ovulation. Progesterone has an antialdosterone effect. The concentrations of certain female sex hormones in the blood plasma depend on the phase of the menstrual cycle.

Ovarian-menstrual (menstrual) cycle

The menstrual cycle ensures the integration over time of various processes necessary for reproductive function: egg maturation and ovulation, periodic preparation of the endometrium for implantation of a fertilized egg, etc. A distinction is made between the ovarian cycle and the uterine cycle. On average, the entire menstrual cycle for women lasts 28 days. Variations from 21 to 32 days are possible. The ovarian cycle consists of three phases: follicular (from the 1st to the 14th day of the cycle), ovulatory (13th day of the cycle) and luteal (from the 15th to 28th day of the cycle). The amount of estrogen predominates in the follicular phase, reaching a maximum one day before ovulation. During the luteal phase, progesterone predominates. The uterine cycle consists of 4 phases: desquamation (duration 3-5 days), regeneration (up to 5-6 days of the cycle), proliferation (up to 14 days) and secretion (from 15 to 28 days). Estrogens cause the proliferative phase, during which the endometrial mucosa thickens and its glands develop. Progesterone promotes the secretory phase.

The production of estrogen and progesterone is regulated by gonadotropic hormones of the adenohypophysis, the production of which increases in girls aged 9-10 years. With a high level of estrogen in the blood, the secretion of FSH and LH by the adenohypophysis, as well as GnRH by the hypothalamus, is inhibited. Progesterone inhibits FSH production. In the first days of the menstrual cycle, under the influence of FSH, follicle maturation occurs. At this time, the concentration of estrogen also increases, which depends not only on FSH, but also on LH. In the middle of the cycle, LH secretion increases sharply, which leads to ovulation. After ovulation, the concentration of progesterone increases sharply. Negative feedback suppresses the secretion of FSH and LH, which prevents the maturation of a new follicle. Degeneration of the corpus luteum occurs. The level of progesterone and estrogen drops. The central nervous system is involved in the regulation of the normal menstrual cycle. When the functional state of the central nervous system changes under the influence of various exogenous and psychological factors (stress), the menstrual cycle may be disrupted until menstruation ceases.

Insufficient production of female sex hormones can occur when the pathological process directly affects the ovaries. This is the so-called primary hylogonodism. Secondary hypogonadism occurs when the production of gonadotropins by the adenohypophysis decreases, resulting in a sharp decrease in the secretion of estrogen by the ovaries. Primary ovarian failure can be congenital due to disorders of sexual differentiation, as well as acquired as a result of surgical removal of the ovaries or damage by an infectious process (syphilis, tuberculosis). If the ovaries are damaged in childhood, there is underdevelopment of the uterus, vagina, primary amenorrhea (absence of menstruation), underdevelopment of the mammary glands, absence or scant hair on the pubis and under the arms, eunuchoid proportions: narrow pelvis, flat buttocks. When the disease develops in adults, the underdevelopment of the genital organs is less pronounced. Secondary amenorrhea occurs, and various manifestations of vegetative neurosis are noted.

Placenta. Epiphysis Thymus

Placenta

The placenta is a temporary organ that forms during pregnancy. It ensures the connection of the fetus with the mother’s body: it regulates the supply of oxygen and nutrients, and the removal of harmful decay products. The placenta also performs a barrier function, protecting the fetus from substances harmful to it.

So, by the 16th week of pregnancy, the corpus luteum in the ovary has practically disappeared. The placenta took all care of hormonal production. It provides the child’s body with the necessary proteins and hormones. Look how impressive their range is: progesterone, estrogen precursors, human chorionic gonadotropin, chorionic somatotropin, chorionic thyrotropin, adrenocorticotropic hormone, oxytocin. relaxin.

Placental hormones ensure normal pregnancy. Chorionic gonadotropin is the most studied. In its physiological properties it is close to pituitary gonadotropins. The hormone has an effect on the differentiation processes and development of the fetus, as well as on the mother’s metabolism: it retains water and salts, stimulates the production of antidiuretic hormone and itself has an antidiuretic effect, stimulates immune mechanisms. Due to the close functional connection between the placenta and the fetus, it is customary to speak of the “fetoplacental complex” or “fetoplacental system”.

The fact is that both the fetus and the placenta individually are imperfect systems due to a lack of enzymes necessary for the independent synthesis of steroid hormones that are extremely important for the entire pregnancy: progesterone and estrogens. Whether it's together! And the baby’s tiny adrenal glands “support” the placenta with all their might. For example, the synthesis of estriol in the placenta comes from the precursor dehydroepiandrosterone, which is formed in the adrenal glands of the fetus. The two enzyme systems work in harmony, complementing each other and forming a single functional hormonal “community”.

After the baby is born, the placenta separates from the walls of the uterus and the placenta is born (within about 30 minutes). It consists of the placenta, umbilical cord and membranes. The separated placenta descends into the vagina, and then, when the woman in labor strains, she is born. Separation of the placenta is accompanied by slight (up to 250 ml) bleeding. The afterbirth is carefully examined by a doctor to determine the integrity of the placenta and membranes.

Pineal gland

The epiphysis (superior medullary appendage, pineal gland, pineal gland) is a gland of neuroglial origin. Produces primarily serotonin and melatonin, as well as norepinephrine and histamine. Peptide hormones and biogenic amines were found in the pineal gland, which allows its cells (pinealocytes) to be classified as cells of the APUD system. For example, it produces arginine-vasotocin (stimulates the secretion of prolactin); pineal hormone, or Milku factor; epithalamin - total peptide complex, etc.

The main function of the pineal gland is the regulation of circadian (daily) biological rhythms, endocrine functions and metabolism and the body's adaptation to changing light conditions. Excess light inhibits the conversion of serotonin to melatonin and other methoxyindoles and promotes the accumulation of serotonin and its metabolites. In the dark, on the contrary, melatonin synthesis increases. This process occurs under the influence of enzymes, the activity of which also depends on illumination. Considering that the pineal gland regulates a number of important reactions of the body, and due to changes in illumination, this regulation is cyclical, it can be considered a regulator of the “biological clock” in the body.

The effect of the pineal gland on the endocrine system is mainly inhibitory in nature. The effect of its hormones on the hypothalamic-pituitary-gonadal system has been proven. Melatonin inhibits the secretion of gonadotropins both at the level of secretion of liberins of the hypothalamus and at the level of the adenohypophysis. Melatonin determines the rhythm of gonadotropic effects, including the duration of the menstrual cycle in women. Pineal gland hormones inhibit the bioelectrical activity of the brain and neuropsychic activity, providing a hypnotic, analgesic and sedative effect. In the experiment, pineal gland extracts cause insulin-like (hypoglycemic), parathyroid-like (hypercalcemic) and diuretic effects.

Thymus

The thymus, or thymus gland, is a paired organ located in the upper mediastinum. After 30 years, it undergoes age-related involution. In the thymus gland, along with the formation of T-lymphocytes from bone marrow stem cells, hormonal factors are produced - thymosin and thymopoietin. Hormones ensure the differentiation of T lymphocytes and play a role in cellular immune responses. There is also evidence that hormones ensure the synthesis of cellular receptors for mediators and hormones, for example, acetylcholine receptors on the postsynaptic membranes of neuromuscular synapses.

Other organs also have endocrine activity. The kidneys synthesize and secrete renin and erythropoietin into the blood. Natriuretic hormone, or ampuonenmud, is produced in the atria. Cells of the mucous membrane of the stomach and duodenum secrete a large number of peptide compounds, a significant part of which are also detected in the brain: secretin, gastrin, cholecystokinin-pancreozymin, gastroinhibitory peptide, bombesin, motilin, somatostatin, neurotensin, pancreatic polypeptide, etc. More details about these substances presented in the relevant sections of the textbook.

Hormonal agents used for pharmacological purposes

Many hormones are used in medical practice as replacement therapy for hypofunction of the corresponding endocrine glands, as well as in the treatment of certain pathological processes. Hormones that do not have species specificity are used in the form of extracts isolated from the body of animals. The establishment of the chemical structure of endogenous hormones made it possible to carry out the targeted synthesis of both the hormones themselves and their active analogues and antihormones. Hormones obtained synthetically, as well as their analogues, have a more selective effect, exert their effects in smaller doses, and therefore cause fewer side effects.

For example, the hormonal drug pituitrin, which has oxytocin (uterine), vasopressor and antidiuretic activity, is obtained from the posterior lobe of the pituitary gland of cattle and pigs. Synthetically produced oxytocin has a more selective effect on the uterus and is used to induce and stimulate labor.

Adiurecrin, a drug from the posterior pituitary gland, the main active ingredient of which is vasopressin, is used to treat diabetes insipidus. Corticotropin (prescribed for hypofunction of the adrenal cortex) and lactin, which has prolactin activity (stimulates lactation in the postpartum period), are obtained from the anterior lobe of the pituitary gland. To accelerate growth, pharmacological drugs somatotropin and human somatotropin are used, since these hormones are species specific. Medicines with FSH activity include menopausal gonadotropin, obtained from the urine of menopausal women, and with LH activity, human chorionic gonadotropin, isolated from the urine of pregnant women.

For hypothyroidism, a hormonal drug from the thyroid glands of slaughter cattle, thyroidin (thyroxine and triiodothyronine) and a synthetic drug triiodothyronine, are used. To treat diabetes mellitus, insulin from the pancreas of pigs and humans is used. In case of insufficient ovarian function, estrone (folliculin) isolated from the urine of pregnant women and animals is used. The synthetic hormone progesterone is prescribed for infertility and miscarriage. The ability of progestins to block the release of releasing factors of the hypothalamus, inhibit the secretion of gonadotropic hormones by the pituitary gland and inhibit ovulation was the basis for the use of progestins as contraceptives. The contraceptive effect is enhanced by the combined use of progestins with estrogens. For sexual dysfunction in men, the synthetic hormone testosterone or a synthetic analogue of methyltestosterone is used.

The most widely used hormones in medical practice are the hormones of the adrenal cortex - corticosteroids, currently obtained synthetically: mineralocorticoid - deoxycorticosterone acetate and glucocorticoids - cortisone, hydrocortisone. More active than natural glucocorticoids are their synthetic analogues (prednisone, prednisolone, dexamethasone). They are used not only for hypofunction of the adrenal cortex, but also as anti-inflammatory, antiallergic agents, and as immunosuppressants during organ and tissue transplantation to inhibit the rejection reaction. The introduction of these substances in large quantities can cause the effects of glucocorticoids described above, but in a more pronounced form, and be a side effect of these substances. So, it must be taken into account that, while suppressing inflammatory processes, glucocorticoids simultaneously weaken the body’s protective immune reactions.

An undesirable side effect is also the inhibition of scar formation during the healing of stomach ulcers or other internal tissue damage. Since glucocorticoids stimulate the secretion of hydrochloric acid, they should not be prescribed to patients with gastric ulcers. Destruction of the protein matrix of bones can lead to a pathological condition - osteoporosis. With long-term treatment with glucocorticoids, a prediabetic state may develop, including diabetes mellitus (steroid diabetes), since these substances are insulin antagonists.

Knowledge of the biorhythms of hormone secretion must be taken into account in clinical practice when distributing the daily dose of hormones. In addition, during long-term treatment with corticoid hormones, it must be remembered that these medications cannot be abruptly discontinued, since long-term treatment with exogenous corticoids inhibits the production of ACTH by the adenohypophysis through a negative feedback mechanism. Under these conditions, the adrenal cortex’s production of its own endogenous corticoids is weakened or even completely stopped. If the administration of exogenous corticoids is abruptly stopped, acute adrenal insufficiency develops, which can be fatal. This pathological condition is called “withdrawal syndrome”. To prevent adrenal atrophy, corticotropin must be prescribed simultaneously.

Parathyroid glands (glandulae parathyroideae; synonym: parathyroid glands, parathyroid glands, epithelial bodies) are endocrine glands that produce a hormone involved in the regulation of calcium and phosphorus metabolism.

A person usually has two pairs of parathyroid glands - superior and inferior, but the number of parathyroid glands can vary from 4 to 12. Superior parathyroid glands. located on the posterior surface of the thyroid gland, at the level of the upper poles of its lobes, outside the capsule. The inferior parathyroid glands are located, as a rule, at the level of the lower poles of the lobes of the thyroid gland, however, the parathyroid glands of this pair, like the accessory parathyroid glands, can be located in the thickness of the thyroid gland, under its capsule, in the anterior or posterior mediastinum, at the thymus, behind esophagus, near the carotid artery at its bifurcation, etc.

The parathyroid glands have a round or elongated shape, they are slightly flattened, the length of each gland is from 2 to 8 mm, width is 3-4 mm, thickness is from 1.5 to 3 mm. The mass of all parathyroid glands. on average is about 0.5 g (the mass of the lower panties is always greater than the mass of the upper ones).

Each parathyroid gland is covered with a thin connective tissue capsule, from which septa extend into the gland, containing blood vessels and vasomotor nerve fibers. The blood supply to the parathyroid glands is carried out mainly by the inferior thyroid artery; venous blood from the parathyroid glands is collected in the veins of the thyroid gland, trachea and esophagus. Each parathyroid gland is innervated by sympathetic fibers of the upper and lower cervical, as well as the stellate ganglia of the sympathetic trunk of its half, and parasympathetic innervation is provided by the vagus nerve.

Parenchyma of the parathyroid glands. an adult human consists mainly of the so-called main parathyrocytes, among which dark main and light main cells are distinguished, and a small number of parathyrocytes that are selectively stained with acid dyes - the so-called acidophilic parathyrocytes. In the parenchyma of the parathyroid glands. You can find cells of a transitional type between the main and acidophilic parathyroid cells, which are most often located along the periphery of the glands. There are also parathyrocytes, called “empty” cells (the so-called watery cells). The main parathyroid cells form clusters, cords and clusters, and in elderly people - follicles with a homogeneous colloid. The tissue of the parathyroid glands may contain K-cells that produce calcitonin (see Thyroid gland); they are found mainly in the pericapillary zone of the lower parathyroid glands.

The physiological significance of the parathyroid gland is its secretion of parathyroid hormone, which, together with calcitonin, which is its antagonist, and vitamin D, is involved in the regulation of calcium and phosphorus metabolism in the body. Parathyroid hormone (parathyroid hormone, parathyroidocrine, parathyrin, calcitrin) is a polypeptide with a molecular weight of about 9500, built of 84 amino acid residues.

Regulation of the activity of the parathyroid glands is carried out according to the feedback principle, the regulating factor is the calcium content in the blood, the regulating hormone is parathyroid hormone. The main stimulus for the release of parathyroid hormone into the bloodstream is a decrease in the concentration of calcium in the blood (normal 2.25-2.75 mmol/l, or 9-11 mg/100 ml). The target organs for parathyroid hormone are the skeleton and kidneys; parathyroid hormone also affects the intestines, enhancing calcium absorption. In the bones, parathyroid hormone activates resorptive processes, which is accompanied by the entry of calcium and phosphates into the blood (which is responsible for the increase in calcium concentration in the blood under the influence of parathyroid hormone). The effect of parathyroid hormone on osteoclasts is inhibited by calcitonin. Demineralization of bone tissue with an excess of parathyroid hormone is accompanied by an increase in the activity of alkaline phosphatase in the blood serum (see Phosphatases) and an increase in the excretion of hydroxyproline (a specific component of collagen) in the urine due to resorption of the organic bone matrix under the influence of parathyroid hormone. In the kidneys, parathyroid hormone reduces phosphate reabsorption in the distal renal tubules. A significant increase in the excretion of phosphates in the urine (phosphaturic effect of parathyroid hormone) is accompanied by a decrease in phosphorus levels in the blood. Despite a slight increase in calcium reabsorption in the renal tubules under the influence of parathyroid hormone, urinary calcium excretion ultimately increases due to increasing hypercalcemia. Under the influence of parathyroid hormone, the formation of the active metabolite of vitamin D, 1,25-dioxycholecalciferol, is stimulated in the kidneys, which increases the absorption of calcium from the intestine. Thus, the effect of parathyroid hormone on the absorption of calcium from the intestine may not be direct, but indirect.

Parathyroid hormone reduces calcium deposition in the lens (with a lack of this hormone, cataracts occur), has an indirect effect on all calcium-dependent enzymes and the reactions they catalyze, incl. on reactions that form the blood coagulation system. Parathyroid hormone is metabolized mainly in the liver and kidneys; its excretion through the kidneys does not exceed 1% of the hormone introduced into the body. The biological half-life of parathyroid hormone is 8-20 minutes.

The functional activity of the parathyroid glands is examined by determining the content of parathyroid hormone in the blood serum. The radioimmunological research method is the most informative, however, it also has certain limitations, since parathyroid hormone in the bloodstream is heterogeneous and is represented by a number of peptides. The level of parathyroid hormone in the blood is considered normal in the range from 0.15 to 0.6-1.0 pg/ml. The adjustability of the function of the parathyroid gland and the degree of its autonomy (during tumor processes) are assessed by changes in the concentration of parathyroid hormone in the blood during loads with calcium preparations and a decrease in the calcium content in a test with calcitrin (calcitonin). Since changes in the function of the parathyroid gland are accompanied by characteristic biochemical changes, for its indirect assessment the concentration of total calcium and ionized Ca2+ and inorganic phosphorus in the blood serum, the excretion of calcium and phosphates in the urine per day are determined, the reabsorption of phosphates in the distal parts of the renal tubules and the activity of alkaline phosphatase in the blood are determined. blood serum. With hyperfunction of the parathyroid gland, an increase in the concentration of total and ionized calcium and a decrease in the concentration of phosphorus in the blood, excessive excretion of calcium in the urine, a decrease in the relative value of tubular reabsorption of phosphates, and an increase in the activity of alkaline phosphatase in the blood serum are detected. With hypofunction of the parathyroid gland, hypocalcemia, hypophosphatemia, hypocalciuria and hypophosphaturia are noted. Nevertheless, the complexity and variety of mechanisms that control the homeostasis of calcium and phosphorus require in each case a comprehensive assessment of all theoretically possible factors involved in the process of regulation of phosphorus-calcium metabolism (see Mineral metabolism). Parathyroid hormone stimulates adenylate cyclase and enhances the renal excretion of cyclic 3,"5"-AMP (cAMP); the content of cAMP in daily urine can serve as an indicator of the state of pancreas function. Loading with calcium salts in healthy people suppresses the secretion of parathyroid hormone and the excretion of cAMP; in hyperparathyroidism, it does not change these indicators; in hypoparathyroidism, the excretion of cAMP after a load with calcium salts decreases and reaches normal only after the administration of parathyroid hormone.

For the differential diagnosis of hypercalcemia, a so-called steroid suppression test is used (hypercalcemia not associated with increased secretion of parathyroid hormone can be eliminated with corticosteroids); a test with a load of thiazide diuretics, which suppress calciuria, which in hyperparathyroidism leads to a sharp increase in the concentration of calcium in the blood, while this is not observed in persons without hyperparathyroidism; calcium tolerance test (when calcium supplements are administered to a patient with hyperparathyroidism, the function of the parathyroid gland does not change; in other cases, the secretion of parathyroid hormone is suppressed); test with calcitrin (calcitonin), which increases the concentration of parathyroid hormone and reduces, but not to normal values, the calcium content in the blood in hyperparathyroidism, but does not affect the concentration of parathyroid hormone in hypercalcemia of another origin, etc. As a rule, several various samples.

To anatomically characterize the parathyroid glands and determine their location, radiography (tomography) of the retrosternal space is used with contrasting the esophagus with a barium suspension (Rehberg-Zemtsov test), radionuclide scanning of the parathyroid glands with 75Se-selenomethionine, ultrasound, computed tomography, thermography, as well as selective arteriography, venous catheterization with selective blood sampling to determine the concentration of parathyroid hormone.

Pineal gland, its hormonal functions

Interesting facts about the pineal gland

Synthesis of scientific and esoteric knowledge about the pineal gland

Then it turns out that the human body, through the pineal gland or other organ, is quite tightly coupled with geo- and heliocosmic processes. And wasn’t it this connection between man and the Cosmos through the pineal gland that the ancient mystics meant when they called the pineal gland the “Spiritual Eye”?

Meanwhile, histochemists tried to figure out the nature and meaning of “brain sand.” Sand grains range in size from 5 microns to 2 mm, often shaped like a mulberry, that is, they have scalloped edges. They consist of an organic base - a colloid, which is considered the secretion of pinealocytes, impregnated with calcium and magnesium salts, mainly phosphates. Using X-ray crystallographic analysis, it was shown that calcium salts in the diffractograms of the pineal gland are similar to hydroxyapatite crystals. Brain grains of sand in polarized light exhibit birefringence with the formation of a “Maltese” cross. Optical anisotropy indicates that the crystals of salt deposits of the pineal gland are not crystals of the cubic system. Due to the presence of calcium phosphate, sand grains primarily fluoresce in ultraviolet rays, like colloid droplets, with a bluish-white glow. A similar blue fluorescence is produced by the myelin sheaths of nerve trunks. Typically, salt deposits have the character of rings - layers alternating with layers of organic matter. Scientists have not yet been able to find out more about “brain sand”.

Now is the time to return to the Secret Doctrine. Elena Petrovna writes the following: “...Morgagni, Grading and Gam were wise people of their generation, and today they are also such, since they are still the only physiologists who..., summing up the facts, that they (grains of sand) are absent in small children , in the aged and in the feeble-minded, the inevitable conclusion was drawn that they (the grains of sand) must be connected with the mind." Even more intimate information is provided by E.I. Roerich in a letter to Dr. A. Aseev: “...a luminous substance, like sand, observed on the surface of the pineal gland in a developed person. This sand is a mysterious substance, which is a deposit of Psychic Energy. Deposits of Psychic Energy can be found in many organs and nerves channels". A very serious selection of calcium metabolism in the body was made by V.T. Volkov in his monograph on bronchial asthma. He was able to detect calcium phosphates in nasopharyngeal lavages from asthmatics, in kidney stones, etc. he hypothesizes that the Charcot-Leyden crystals are apatites. It is very possible that calcium phosphates are deposited in the prepuce glands of musk rams as a carrier of Psychic Energy. This topic in medicine and biology is still waiting for its researchers.

Pineal gland, its hormonal functions

EPIPHYSUS (pineal, or pineal, gland), a small formation located in vertebrates under the scalp or deep in the brain; functions either as a light-sensing organ or as an endocrine gland, the activity of which depends on illumination. In some vertebrate species both functions are combined. In humans, this formation is shaped like a pine cone, which is where it got its name (Greek epiphysis - cone, growth).

The pineal gland develops in embryogenesis from the fornix (epithalamus) of the posterior part (diencephalon) of the forebrain. Lower vertebrates, such as lampreys, may develop two similar structures. One, located on the right side of the brain, is called the pineal gland, and the second, on the left, is the parapineal gland. The pineal gland is present in all vertebrates, with the exception of crocodiles and some mammals, such as anteaters and armadillos. The parapineal gland as a mature structure is present only in certain groups of vertebrates, such as lampreys, lizards and frogs.

Function. Where the pineal and parapineal glands function as a light-sensing organ, or "third eye", they are only able to distinguish between different degrees of illumination, and not visual images. In this capacity, they can determine certain forms of behavior, for example, the vertical migration of deep-sea fish depending on the change of day and night.

In amphibians, the pineal gland performs a secretory function: it produces the hormone melatonin, which lightens the skin of these animals, reducing the area occupied by pigment in melanophores (pigment cells). Melatonin is also found in birds and mammals; it is believed that in them it usually has an inhibitory effect, in particular, it reduces the secretion of pituitary hormones.

In birds and mammals, the pineal gland plays the role of a neuroendocrine transducer, responding to nerve impulses by producing hormones. Thus, light entering the eyes stimulates the retina, impulses from which travel along the optic nerves to the sympathetic nervous system and pineal gland; these nerve signals cause inhibition of the activity of the epiphyseal enzyme necessary for the synthesis of melatonin; as a result, the latter's production ceases. On the contrary, in the dark, melatonin begins to be produced again.

Thus, cycles of light and dark, or day and night, affect melatonin secretion. The resulting rhythmic changes in its level - high at night and low during the day - determine the daily, or circadian, biological rhythm in animals, including the frequency of sleep and fluctuations in body temperature. In addition, by responding to changes in night length by changing the amount of melatonin secreted, the pineal gland likely influences seasonal responses such as hibernation, migration, molting, and reproduction.

In humans, the activity of the pineal gland is associated with such phenomena as disruption of the body’s circadian rhythm due to flying across several time zones, sleep disorders and, probably, “winter depression.”

The pineal body (epiphysis, pineal gland, superior cerebral appendage) is a small oval glandular formation that belongs to the diencephalon and is located in a shallow groove between the superior colliculi of the midbrain and above the thalamus.
The weight of the gland in an adult is about 0.2 g, length 8-15 mm, width 6-10 mm, thickness 4-6 mm.

On the outside, the pineal body is covered with a soft connective tissue membrane of the brain, which contains many anastomosing (connecting to each other) blood vessels. The cellular elements of the parenchyma are specialized glandular cells - pineocytes and glial cells - gliocytes.

The pineal gland produces primarily serotonin and melatonin, as well as norepinephrine and histamine. Peptide hormones and biogenic amines were found in the pineal gland. The main function of the pineal gland is the regulation of circadian (daily) biological rhythms, endocrine functions, metabolism (metabolism) and the body’s adaptation to changing light conditions.

Melatonin determines the rhythm of gonadotropic effects, including the duration of the menstrual cycle in women. This hormone was originally isolated from the pineal bodies of cattle, and, as it turned out, has an inhibitory effect on the function of the gonads, or rather inhibits the growth hormone secreted by another gland (pituitary gland). After removal of the pineal gland, chickens experience premature puberty (the same effect occurs as a result of a tumor of the pineal gland). In mammals, removal of the pineal body causes an increase in body weight, in males - hypertrophy (enlargement) of the testes and increased spermatogenesis, and in females - an extension of the life span of the ovarian corpus luteum and an enlargement of the uterus.

Excess light inhibits the conversion of serotonin to melatonin. In the dark, on the contrary, melatonin synthesis increases. This process occurs under the influence of enzymes, the activity of which also depends on illumination. This explains the increase in sexual activity of animals and birds in spring and summer, when, as a result of increasing day length, the secretion of the pineal gland is suppressed. Considering that the pineal gland regulates a number of important reactions of the body, and due to changes in illumination, this regulation is cyclical, it can be considered a regulator of the “biological clock” in the body.

Pineal gland hormones inhibit the bioelectrical activity of the brain and neuropsychic activity, providing a hypnotic and calming effect.

A small outgrowth of the brain, hidden under the cerebral hemispheres, is called the pineal gland due to its appearance. A body in the form of a pine cone was once depicted in those parts of the papyri where it was said about the entry of the souls of the deceased into the judgment hall of Osiris. The very archaic meaning of a cone (and “cones” can be important) is a symbol of eternal life, as well as restoration of health.

The functions of this gland remained unclear for many, many years. Some regarded the gland as a vestigial eye, previously intended to help a person protect himself from above. But such a gland, the pineal gland, can be recognized as a structural analogue of the eye only in lampreys, in reptiles, and not in us. In mystical literature there was periodically a statement about the contact of this particular gland with a mysterious immaterial thread connecting the head with the ethereal body hovering above each.

From essay to essay, a description of this organ migrated, supposedly capable of restoring images and experiences of a past life, regulating the flow of thought and the balance of the intellect, and carrying out telepathic communication. The French philosopher R. Descartes (17th century) believed that the gland performs mediating functions between spirits, that is, impressions coming from paired organs - eyes, ears, hands. Here, in the pineal gland, under the influence of “blood vapors,” anger, joy, fear, and sadness are formed. The imagination of the great Frenchman endowed the gland with the ability not only to move, but also to direct “animal spirits” through the pores of the brain along the nerves to the muscles. It was later discovered that the pineal gland was unable to move.

For a number of years, proof of the exclusivity of the pineal gland was the fact that the heart also does not have a pair, but lies “in the middle.” Yes, and the pineal gland exists, as Descartes mistakenly assumed, only in humans. In ancient Russian medical manuals this gland was called “spiritual”.

In the twenties of the last century, many experts came to the conclusion that there was no point in talking about this gland, because the supposedly vestigial organ did not have any significant function. Doubts arose that the pineal gland, weighing two hundred milligrams and the size of a pea, functions not only in embryogenesis, but also after birth. All this led to the fact that this “third eye” fell out of the field of view of researchers for a number of decades. True, there were also objective reasons. Among them are the difficulty of studying, which required new methods, and topographical inconvenience - it is very difficult to remove this organ. Theosophists, in turn, had no doubt that the pineal gland is not very necessary for most people, but in the future it will turn out to be necessary for the transmission of thoughts from one person to another.

Synthesis of scientific and esoteric knowledge about the pineal gland

In 1695, in Moscow, the doctor V. Yurovsky presented a dissertation on the pineal gland for defense. Based on his anatomical studies, the author refuted the views of ancient philosophers about the localization of the mind in the pineal gland. This study can be considered the beginning of an objective, materialistic approach to the study of this mysterious gland. Mysterious because none of the subsequent researchers, based on their work, was able to offer any plausible hypothesis about the role of the pineal gland in the body.

Basic information about the physiological significance of the pineal gland has been obtained by science in recent decades. The gland is located in the center of the brain, in the back of the third ventricle. Its length rarely exceeds 10 mm, and its width and height are 7 and 4.5 mm, respectively. Cells similar to the pigment cells of the retina and melanocytes of the skin are located here. Already in our time it has been found that these cells - pinealocytes - secrete serotonin during daylight hours, and in the dark - these same cells begin to synthesize another tryptophan derivative. This substance was identified in 1958 as the pineal gland hormone - melatonin. It is believed that the pineal gland secretes other hormones. Information to the organ about the degree of external illumination comes from the retina via sympathetic fibers. And in some animals, such as migratory birds, the pineal gland has the ability to detect changes in light directly through the integument of the skull. In addition, it has been established that the pineal gland acts as a navigation device during flights. In more primitive animals, photoreceptors similar to the receptors in the retina of the eye were found in the pineal gland. Biologists confirm that evolutionarily the pineal gland did not immediately appear in the center of the brain. Initially, it performed the function of the “occipital eye,” and only later, as the brain hemispheres developed, this gland found itself practically in the center. Even in the pineal gland of almost all adults, fairly strong inorganic grains of sand were found - brain sand - deposits of calcium salts. E.P. Blavatsky wrote in The Secret Doctrine: “... this sand is very mysterious and baffles the research of all materialists. Only this sign of the internal independent activity of the pineal gland does not allow physiologists to classify it as an absolutely useless atrophied organ.” This was indeed the case. For example, not so long ago, radiologists proposed using the radiopacity of epiphyseal sand to detect displacements of brain structures during intracranial space-occupying processes. It was only after the discovery of melatonin that scientists again became interested in the pineal gland.

The maximum amount of melatonin is produced at night, the peak of activity occurs at approximately 2 a.m., and by 9 a.m. its content in the blood drops to its minimum values. It has been experimentally established that melatonin, when taken orally, has a hypnotic effect without disturbing the sleep phase, a hypotensive effect, normalization of the body's immune reactions and neutralization of the effects of stress hormones on tissues have been noted. Melatonin has proven to be a powerful natural antioxidant and can be used to prevent cancer. The literature contains data on its effectiveness in bronchial asthma, glaucoma, cataracts, and as a harmless contraceptive. Summarizing the whole range of effects, we can say that melatonin has a rejuvenating effect on the body as a whole. According to the level of secretory activity, three periods are distinguished. The maximum secretion of melatonin was observed in childhood. At 11-14 years of age, a decrease in melatonin production by the pineal gland “triggers” the hormonal mechanisms of puberty. And another significant decrease in gland activity coincides with the onset of menopause.

One of the researchers, Walter Pierpaoli, calls the pineal gland the “conductor” of the endocrine system, since based on his research he came to the conclusion that the activity of the pituitary gland and hypothalamus is controlled by the pineal gland. It also turned out that in diabetes mellitus, depression and cancer, melatonin synthesis is reduced or the normal rhythm of its secretion is disrupted. Taking the hormone for these diseases led to positive results.

In addition, the impact of environmental factors on the level of endogenous melatonin secretion was studied. They found that melatonin synthesis stops in bright light. This discovery sparked a renaissance in phototherapy. And now phototherapy in the West is widely used by chronobiologists to treat desynchronosis. It turned out that reducing the diet of experimental animals by 60% leads to an increase in life expectancy by 1.5 times. And in humans, a low-calorie diet slows down the aging process, reduces the likelihood of developing all the diseases that most often kill people in developed countries (cancer, heart disease, strokes, atherosclerosis, diabetes). At the same time, special studies have established that it is the pineal gland that responds to dietary restrictions, increasing the secretion of melatonin. Life expectancy is related to the total amount of hormone synthesized at night. And the work of the endocrine system as a whole is very sensitively programmed in childhood, depending on the nutritional culture. It was also found that dosed hypoxia and physical activity help normalize the disturbed rhythm of melatonin secretion.

It may turn out that it is the pineal gland that is capable of detecting changes in the electromagnetic background. This assumption is supported by a number of facts:

• For migratory birds, the pineal gland is a navigation device.
• When the human body is exposed to the electromagnetic field of working household and industrial electrical appliances, the antitumor effect of melatonin is reliably inhibited.
• Correlation of the nocturnal peak of melatonin secretion with nocturnal pulses of the Earth's magnetic field, around 2 am
• Positive results in the treatment of various diseases with local dosed irradiation of the diencephalon with X-rays

Then it turns out that the human body, through the pineal gland or other organ, is quite tightly coupled with geo- and heliocosmic processes. And wasn’t it this connection between man and the Cosmos through the pineal gland that the ancient mystics meant when they called the pineal gland the “Spiritual Eye”? Meanwhile, histochemists tried to figure out the nature and meaning of “brain sand.” Sand grains range in size from 5 microns to 2 mm, often shaped like a mulberry, that is, they have scalloped edges. They consist of an organic base - a colloid, which is considered the secretion of pinealocytes, impregnated with calcium and magnesium salts, mainly phosphates. Using X-ray crystallographic analysis, it was shown that calcium salts in the diffractograms of the pineal gland are similar to hydroxyapatite crystals. Brain grains of sand in polarized light exhibit birefringence with the formation of a “Maltese” cross. Optical anisotropy indicates that the crystals of salt deposits of the pineal gland are not crystals of the cubic system. Due to the presence of calcium phosphate, sand grains primarily fluoresce in ultraviolet rays, like colloid droplets, with a bluish-white glow. A similar blue fluorescence is produced by the myelin sheaths of nerve trunks. Typically, salt deposits have the character of rings - layers alternating with layers of organic matter. Scientists have not yet been able to find out more about “brain sand”. Now is the time to return to the Secret Doctrine. Elena Petrovna writes the following: “...Morgagni, Grading and Gam were wise people of their generation, and today they are also such, since they are still the only physiologists who..., summing up the facts, that they (grains of sand) are absent in small children , in the aged and in the feeble-minded, the inevitable conclusion was drawn that they (the grains of sand) must be connected with the mind." Even more intimate information is provided by E.I. Roerich in a letter to Dr. A. Aseev: “...a luminous substance, like sand, observed on the surface of the pineal gland in a developed person. This sand is a mysterious substance, which is a deposit of Psychic Energy. Deposits of Psychic Energy can be found in many organs and nerves channels". A very serious selection of calcium metabolism in the body was made by V.T. Volkov in his monograph on bronchial asthma. He was able to detect calcium phosphates in nasopharyngeal lavages from asthmatics, in kidney stones, etc. he hypothesizes that the Charcot-Leyden crystals are apatites. It is very possible that calcium phosphates are deposited in the prepuce glands of musk rams as a carrier of Psychic Energy. This topic in medicine and biology is still waiting for its researchers.

The endocrine system consists of organs and tissues that produce hormones. Hormones are natural chemical substances produced in one place that enter the bloodstream and are then used by other target organs and systems.

Hormones control target organs. Some organs and systems have their own internal control systems instead of hormones.

With age, naturally, changes occur in those body systems that are under control. Some target tissues become less sensitive to their control hormones. The amount of hormones produced by the endocrine system may also change.

The level of some hormones in the blood may increase or decrease slightly, while others remain unchanged. Exchange processes (metabolism), accordingly, can proceed faster or more slowly.

Many of the organs that produce hormones are in turn controlled by other hormones. Aging also changes this process. For example, slower growth of endocrine tissue may cause it to produce less hormones than it did at an earlier age, or it may produce the same amount of hormones, but at a slower rate.

The work of the hypothalamus

The hypothalamus is located in the brain. It produces hormones that control other structures in the endocrine system. The amount of these regulatory hormones remains approximately the same, but the response of endocrine organs to these hormones may change with age.

The work of the pituitary gland

The pituitary gland is also located in the brain. This gland reaches its maximum size in middle age and then gradually decreases. It consists of three parts: front, intermediate and rear.

The anterior part produces hormones that affect the thyroid gland, adrenal cortex, ovaries, testes and mammary glands. These hormones regulate the synthesis and secretion of hormones from the pituitary glands according to the feedback principle: when the concentration of a certain hormone in the blood decreases, the cells of the adenohypophysis release a signal hormone that stimulates the formation of the hormone by this gland, and an increase in its level in the blood leads to a slowdown in the secretion of the signal hormone.

In the intermediate part, lipotropic factors of the pituitary gland are produced, which influence the mobilization and utilization of fats in the body.

Thyroid function

The thyroid gland is located in the neck and produces hormones that help control metabolism. As the body ages, the thyroid gland often becomes lumpy (nodular). Metabolism gradually declines starting around age 20. With age, hormone secretion may decrease.

Function of the parathyroid glands

The parathyroid glands are four tiny glands located around the thyroid gland. They produce parathyroid hormone, which is involved in the regulation of calcium and phosphorus metabolism. This, in turn, affects bone strength. Changes in parathyroid hormone levels may contribute to osteoporosis.

The work of the pancreas

Insulin, a hormone produced by the pancreas. The insulin molecule binds to a specific glycoprotein receptor on the surface of the target cell. It acts like a key in a lock to help sugar (glucose) move from the blood into cells where it can be used for energy.

Average fasting glucose levels increase from 6 to 14 mg/dL (milligrams per deciliter) for every 10 years after age 50. This is because the cells become less sensitive to the effects of insulin, likely due to the loss of insulin receptors in the cell wall.

Adrenal gland function

The adrenal glands are located just above the kidney. The adrenal cortex, its superficial layer, produces the hormones aldosterone and cortisol.

Aldosterone regulates water-salt balance.

Cortisol is the "stress" hormone. It affects the breakdown of glucose, proteins and fats, and also has an anti-inflammatory and anti-allergenic effect.

The secretion of aldosterone decreases with age, this can contribute to the appearance of dizziness and a decrease in blood pressure during a sharp transition from a horizontal to a vertical state of the body (orthostatic hypotension).

Cortisol secretion also decreases with age, but blood levels remain approximately the same. Dehydroepiandrosterone levels also drop, although the effects of this drop on the body are unclear.

Function of the gonads

The ovaries and testes have two functions. They produce sex cells (eggs and sperm). They also produce sex hormones that control the development of secondary sexual characteristics, such as breasts and facial and body hair. As men age, they sometimes experience a decrease in testosterone levels. Women experience a decrease in estradiol and other estrogen hormones after menopause.

The effect of hormone changes on the body

In general, some hormones decrease, some remain unchanged, and some increase with age.

Hormones that typically decline with age:

Aldosterone
- Calcitonin
- A growth hormone
- Renin
- In women, estrogen and prolactin.

Hormones that remain unchanged or decrease slightly:

Cortisol
- Adrenaline
- Insulin
- Thyroid hormones T3 and T4
- In men, testosterone levels usually decline slightly as they age.

Hormones that may increase in production with age:

Follicle stimulating hormone (FSH)
- Luteinizing hormone (LH)
- Norepinephrine
- Parathyroid hormone.

Endocrine system n 1. Endocrine glands n PITUITARY GLANDS (adenohypophysis and neurohypophysis) n ADRENAL GLANDS (cortex and medulla) n THYROID GLAND n PARATHYROID GLANDS n EPIPHYSUS n 2. Organs with endocrine tissue n PANCREAS n GENITAL GLANDS n 3. Organs with endocrine cell function n PLACENTA n THYMUS n KIDNEYS n HEART

General properties of the endocrine glands: n 1) the absence of external ducts, the produced hormones enter directly into the blood; n 2) small size and weight of the glands; n 3) exposure to low concentrations; n 4) selectivity of hormone action; n 5) specificity of the caused functional effects; n 6) rapid destruction of hormones.

The chemical nature of hormones n steroid – sex hormones and hormones of the adrenal cortex; n amino acid derivatives – hormones of the adrenal medulla and thyroid gland; n protein-peptide hormones – hormones of the pituitary gland, pancreas, parathyroid glands, as well as hypothalamic neuropeptides.

MALE SEX HORMONES TESTOSTERONE, ANDROSTERONE Sexual differentiation in ontogenesis Regulation of sexual behavior Development of sexual characteristics Regulation of spermatogenesis Anabolic effect on the skeleton and muscles of the body Retention of nitrogen, K, P and calcium in the body Activation of RNA synthesis Stimulation of erythropoiesis

FEMALE SEX HORMONES ESTROGENS Sexual differentiation in embryogenesis, puberty, development of female sexual characteristics, establishment of the menstrual cycle Growth of the muscle and epithelium of the uterus, stimulation of the proliferative phase of the cycle Regulation of sexual behavior Increased contractility of the uterus and its sensitivity to oxytocin Development of the mammary glands Weak anabolic effect PROGESTERONE Maintenance of pregnancy Weakening the readiness of the uterus to contract Activation of the secretory structures of the endometrium Activation of the growth of the mammary glands Suppression of the secretion of gonadotropins by the pituitary gland

The negative effect of excessive release of glucocorticoids leads to negative effects: n immunity decreases (the production of antibodies and lymphocytes, the intensity of phagocytosis decreases); n the risk of gastric ulcers increases as a result of activation of the secretion of hydrochloric acid and pepsin in the stomach; n at high concentrations, glucocorticoids behave like aldosterone and activate the process of reabsorption of water and sodium ions, causing their retention in the body, which leads to an increase in blood pressure; n increase the sensitivity of vascular smooth muscles to catecholamines, which leads to spasm of blood vessels, especially small ones, and accordingly to an increase in blood pressure; n cause demineralization of bones, loss of calcium in the urine, reduce calcium absorption in the intestine; n as a result of active gluconeogenesis, the process of protein synthesis in skeletal muscles is inhibited and muscle weakness appears.

Changes in the endocrine glands occur heterochronically, that is, at different times. Thus, the function of the pituitary gland is preserved until old age.

Significant changes in its structure are observed in the thyroid gland. The weight of the gland is reduced due to the replacement of part of the glandular tissue with adipose tissue. The rate of iodine accumulation in the iron decreases. Oxygen consumption by glandular tissue decreases, which leads to a decrease in the synthesis of thyroid hormones, while at the same time the sensitivity of tissues and organs to humoral factors increases, including thyroid hormones.

Consequently, self-regulation processes in the body are maintained at a high level for quite a long time.

The female reproductive glands are the ovaries.

With age, the size and shape of the ovaries changes. They reach their maximum weight by the age of 30. After 40 years, there is a progressive decrease in the mass of the ovaries, they change their shape, undergo atrophy and fibrosis.

Despite the changes occurring, the ovaries retain the ability to produce estrogen for a long time. Due to estrogens, proliferative processes in the mucous membrane of the uterus and vagina are supported, the shape of the mammary glands is preserved, and secondary sexual characteristics are preserved.

With the onset of menopause, estrogen production drops sharply, and this leads to regression of secondary sexual characteristics. Against this background, rapid development of atherosclerosis, osteoporosis, and deforming osteoarthritis is possible.

Male gonads - testicles.

Age-related changes in the male reproductive glands occur at a later age than in women and occur at a slower pace. The male gonads reach their greatest mass by the age of 25–30, after which they slightly decrease in mass. Age-related changes that occur in them lead to a decrease in spermatogenesis, but this is purely individual. Gerontologists noted that even very old people have normal, active sperm in their semen.

With age, obliteration of the seminiferous tubules is observed in the testicles. The number of Leydig cells responsible for the production of androgens decreases. Therefore, with the aging of the gonads in men, there is a decline in secondary sexual characteristics, gynecomastia appears, the timbre of the voice changes, the development of female-type obesity is possible, and the growth of mustaches and beards slows down. Mental weakness and decreased physical strength may develop.

Factors accelerating the aging of the endocrine system:

Smoking,

Alcoholism,

substance abuse,

surgical interventions,

viral infections,

use of medications