Hormonal function of the pituitary gland

STG is a peptide isolated from the anterior pituitary gland and consists of 191 amino acids. The daily production of STH is approximately 500 μg. STG stimulates protein synthesis, mitosis processes of cells and enhances lipolysis. The half-life of STH in adults is 25 minutes. Inactivation of the hormone in the blood is carried out by hydrolysis. In comparison with other hormones, STH is present in the pituitary gland in the largest amount( 5-15 mg / g of tissue).The main function of STH is stimulation of body growth. STG promotes protein synthesis and, interacting with insulin, stimulates the flow of amino acids into cells. It also affects the absorption and oxidation of glucose by fatty tissue, muscles and liver. STG increases the sensitivity of adipocytes to the lipolytic action of catecholamines and reduces their sensitivity to the lipogenic action of insulin. These effects lead to the release of fatty acids and glycerin from adipose tissue into the blood, followed by their metabolism in the liver. STH reduces esterification of fatty acids, thereby reducing the synthesis of TG.Current data suggest that the STH can reduce glucose consumption by fatty tissue and muscles by post-receptor inhibition of insulin action. STG increases the transport of amino acids to the muscle, creating a substrate for protein synthesis. Through a separate mechanism, the STH increases the synthesis of DNA and RNA.

STH stimulates cell growth both directly and indirectly through IGF I and II.The main biological effects of STH are provided by IGFR I.

The secretion of STH normally occurs unevenly. For most of the day, its concentration in the blood of healthy people is very low. For a day there are 5-9 discrete hormone releases. The low initial level of secretion and the pulsating nature of the emissions make it difficult to assess the results of determining the concentration of blood glucose in the blood. In such cases, special provocative tests are used.

The regulation of the secretion of STH is mainly carried out by two peptides of the hypothalamus: STRH, which stimulates the formation of STH, and somatostatin, which has the opposite effect. In the regulation of STH secretion, IGFR also participates. Increase in blood concentration in IGFR I ​​suppresses the transcription of STH genes in pituitary somatotrophs by the negative feedback principle.

Fig. The main metabolic effects of STD

Fig. The main metabolic effects of STD

The main disorders of the somatotropic function of the pituitary gland are represented by excessive or insufficient production of STH.Gigantism and acromegaly are neuroendocrine diseases caused by chronic hyperproduction of STG somatotrophs of the anterior lobe of the pituitary gland. Excessive production of STH in the period of osteogenesis before the closure of the epiphyses leads to gigantism. After the closure of the epiphyses, hypersecretion of STH causes acromegaly. Pituitary gigantism is rarely observed, it occurs at a young age. Acromegaly occurs mainly at the age of 30-50 years( the average frequency is 40-70 cases per 1 million population).

Development of hypophyseal nanism( dwarfism) in the vast majority of cases is associated with a deficiency of somatotropic function of the anterior lobe of the pituitary gland, until its complete loss. Disruption of production of STH by the pituitary gland is most often( approximately 70% of cases) due to the primary damage to the hypothalamus. Congenital aplasia and hypoplasia of the pituitary gland are very rarely detected. Any destructive changes in the hypothalamic-pituitary region can lead to a halt in growth. Most often, they are caused by craniopharyngiomas,

germins, CNS and other tumors of the hypothalamic region, tuberculosis, sarcoidosis, toxoplasmosis, and aneurysms of cerebral vessels.

There are known forms of nanism, mostly hereditary, in which the formation and secretion of STH are not violated. In particular, children with Laron's syndrome have all the signs of hypopituitarism, but the concentration of blood glucose in the blood is increased against the background of a decreased content of IGFR I. The main defect is caused by the inability of STH to stimulate the production of IGFR I.

Many patients with hypopituitarism fail to detect obvious structural damage to the hypothalamusor pituitary gland;in such cases the pathology is more often caused by functional defects of the hypothalamus. Insufficiency of STH can be both isolated and combined with insufficiency of other pituitary hormones.