A 191 amino-acid polypeptide trophic hormone. GH normally has pulsatile secretion (≈ 5–10 pulses/ 24 hours, primarily at night, up to 30 mcg/L), levels may be undetectable (< 0.2 mcg/L) by standard assays between pulses.
Insulin-like growth factor-1 (IGF-1) (formerly known as somatomedin-C) is the protein secreted primarily by the liver in response to GH that is responsible for most of GH’s systemic effects. GH also acts directly on epiphyseal endplates of long bone to stimulate chondrocyte proliferation. Control: GH is under dual hypothalamic control via the hypophysial portal system. GH-releasing hormone (GHRH) from the arcuate nucleus stimulates the pituitary secretion and synthesis of GH and induces GH gene transcription. Somatostatin from the periventricular nucleus suppresses GH release only, and has no effect on synthesis. GH release is also stimulated by ghrelin, a peptide synthesized primarily in the GI tract in response to certain nutrients (may act partially or totally via hypothalamic GHRH).
Growth hormone (GH), also known as somatotropin (or as human growth hormone [hGH or HGH] in its human form), is a peptide hormone that stimulates growth, cell reproduction, and cell regeneration in humans and other animals. It is thus important in human development. It is a type of mitogen which is specific only to certain kinds of cells. Growth hormone is a 191-amino acid, single-chain polypeptide that is synthesized, stored and secreted by somatotropic cells within the lateral wings of the Anterior pituitary.
GH is a stress hormone that raises the concentration of glucose and free fatty acids.
Its clinical application to treatment in various fields, involving obesity, wounds, fractures, gastric ulcers and so on, is being increasingly discussed. The presence or absence of the effect of GH on leukopoiesis was studied in vivo and in vitro experiments. In the in vivo experiment, GH was administered to rats whose bone marrow production had been suppressed by the injection of mitomycin C, and time-course changes in the peripheral blood leukocyte count in these rats were compared with those in rats given physiological saline solution alone (control group). The in vitro experiment was performed by colony assay of mouse marrow cells. Insulin growth factor-1 (IGF-1) was also studied in the in vitro experiment. The in vivo experiment revealed that GH promoted recovery of leukocytes from the nadir, and in the in vitro experiments GH and IGF-1 were demonstrated to increase the number of colonies in the presence of granulocyte macrophage colony stimulating factor (GM-CSF). GH was considered to exert effects on myeloid progenitor cells and the hemopoietic microenvironment simultaneously, resulting in an increase in leukocytes 1).