BACKGROUND Growth hormone (GH) is a member of the somatotropin/prolactin family of hormones. It consists of about 190 amino acids that is synthesized and secreted by cells called somatotrophs in the anterior pituitary. It is a major participant in control of several complex physiologic processes, including growth and metabolism. Multiple signaling pathways mediate the diverse effects of GH. The interaction of GH with GH receptors (GHR) on target cells promotes the association of the cellular tyrosine kinase JAK2 with the GHR, initiating tyrosine phosphorylation of GHR and JAK2, and activation of multiple signaling cascades. GH-stimulated activation of STATs, MAPK and PI-3 kinase cascades have been shown to regulate the transcription of GH-responsive genes. Cross-talk among these signaling cascades in regulating specific genes suggests that GH signaling to the nucleus involves a GH-regulated signaling network.1
GH stimulates both the differentiation and proliferation of myoblasts. It also stimulates amino acid uptake and protein synthesis in muscle and other tissues. Its major role in stimulating body growth is to stimulate the liver and other tissues to secrete IGF-1. IGF-I stimulates proliferation of chondrocytes (cartilage cells), resulting in bone growth. GH does seem to have a direct effect on bone growth in stimulating differentiation of chondrocytes. IGF-I also appears to be the key player in muscle growth. Moreover, GH has important effects on protein, lipid and carbohydrate metabolism. In general, GH stimulates protein anabolism in many tissues. It enhances the utilization of fat by stimulating triglyceride breakdown and oxidation in adipocytes. GH is one of a battery of hormones that serves to maintain blood glucose within a normal range. GH is often said to have anti-insulin activity, because it suppresses the abilities of insulin to stimulate uptake of glucose in peripheral tissues and enhance glucose synthesis in the liver.2 Somewhat paradoxically, administration of GH stimulates insulin secretion, leading to hyperinsulinemia.
Production of GH is modulated by many factors, including stress, exercise, nutrition, sleep and GH itself. However, its primary controllers are two hypothalamic hormones and one hormone from the stomach:3 Growth hormone-releasing hormone (GHRH) is a hypothalamic peptide that stimulates both the synthesis and secretion of GH. Somatostatin (SS) is a peptide produced by several tissues in the body, including the hypothalamus. Somatostatin inhibits GH release in response to GHRH and to other stimulatory factors such as low blood glucose concentration. Ghrelin is a peptide hormone secreted from the stomach. Ghrelin binds to receptors on somatotrophs and potently stimulates secretion of GH. GH secretion is also part of a negative feedback loop involving IGF-I. High blood levels of IGF-I lead to decreased secretion of GH not only by directly suppressing the somatotroph, but by stimulating release of somatostatin from the hypothalamus. GH also feeds back to inhibit GHRH secretion and probably has a direct (autocrine) inhibitory effect on secretion from the somatotroph. Clinically, deficiency in GH or defects in its binding to receptor are seen as growth retardation or dwarfism. The effect of excessive secretion of GH is seen as two distinctive disorders: Giantism and Acromegaly. GH is also of considerable interest as a drug used in both humans and animals.
1. Campbell, G.S.: J Pediatr. 131(1 Pt 2):S42-4, 1997
2. Davidson, M.B.: Endocrine Rev. 8 :115-131, 1987
3. Corpas, E. et al: Endocrine Rev. 14:20-39, 1993
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