Growth hormone (GH)
Also known as: GH, somatotropin, somatotrophin, hGH
A 191-amino-acid protein from somatotrophs that promotes growth (largely by inducing IGF-1) and acts directly as a counter-regulatory, fat-mobilising, insulin-antagonising metabolic hormone.
Overview
GH is the most abundant anterior pituitary hormone. It is secreted in pulses — most strikingly during slow-wave sleep — with peak output during the pubertal growth spurt and a steady decline thereafter (somatopause). About half circulates bound to GH-binding protein (the shed extracellular domain of its receptor).
GH binds a cytokine-family receptor that dimerises and activates JAK2–STAT5. Its effects fall into two groups. Indirect (growth-promoting) effects are mediated by insulin-like growth factor 1 (IGF-1), produced mainly by the liver (endocrine IGF-1) and locally in cartilage and bone (paracrine IGF-1): proliferation of chondrocytes in the epiphyseal growth plate, protein synthesis and positive nitrogen balance, growth of muscle, bone and viscera. Direct (metabolic) effects oppose insulin: lipolysis and fatty-acid oxidation, increased hepatic glucose output and reduced peripheral glucose uptake ("diabetogenic"), plus sodium and water retention. GH is therefore an anabolic hormone for protein but a catabolic, counter-regulatory hormone for fat and carbohydrate, which is why fasting and hypoglycaemia stimulate it.
- Location
Source: somatotrophs of the anterior pituitary. Targets: liver (IGF-1 synthesis), growth plate chondrocytes, muscle, adipose tissue, bone.
Function
- Stimulates linear growth via IGF-1 at the epiphyseal plates (until fusion).
- Increases protein synthesis and lean body mass.
- Mobilises fat (lipolysis) and spares glucose; antagonises insulin.
- Increases bone mineral density and renal Na⁺ retention.
- Physiology
Class: protein (191 amino acids, 22 kDa). Receptor: GH receptor — cytokine receptor/JAK2–STAT5. Half-life ≈20 min. IGF-1 (≈70 % carried by IGFBP-3 and the acid-labile subunit) provides a stable integrated marker of GH status.
- Regulation
Stimulated by GHRH, ghrelin, deep sleep, exercise, fasting, hypoglycaemia, amino acids (arginine), stress, sex steroids at puberty, α2-agonists (clonidine) and glucagon. Inhibited by somatostatin, IGF-1 and GH itself (feedback), hyperglycaemia (basis of the glucose suppression test), raised free fatty acids, obesity, glucocorticoid excess and hypothyroidism.
Clinical significance
GH excess — gigantism and acromegaly
Somatotroph adenoma. Before epiphyseal fusion → gigantism (tall stature); after → acromegaly: coarse features, prognathism, frontal bossing, large hands and feet (rings and shoes no longer fit), macroglossia, sweating, carpal tunnel syndrome, arthropathy, sleep apnoea, impaired glucose tolerance, hypertension, cardiomyopathy and colonic polyps. Diagnosis: raised IGF-1 and failure of GH to suppress below ≈1 µg/L in an OGTT.
GH deficiency
Children: short stature with slow growth velocity, delayed bone age, increased subcutaneous fat, and neonatal hypoglycaemia or micropenis in congenital forms; diagnosed with stimulation tests (insulin tolerance, arginine, glucagon) and treated with recombinant GH. Adults: reduced muscle mass and exercise capacity, central adiposity, dyslipidaemia, reduced bone density and quality of life.
Laron syndrome
GH receptor defect: high GH but very low IGF-1, severe short stature; treated with recombinant IGF-1 (mecasermin).
Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.