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Human Body Study

GH / Somatotropic Axis

The GH / somatotropic axis The hypothalamus controls anterior pituitary GH release with two opposing signals — GHRH stimulates, somatostatin inhibits. Ghrelin from the stomach also stimulates GH. GH acts directly on peripheral tissues and stimulates the liver to release IGF-1, which mediates most growth-promoting effects. IGF-1 and GH feed back negatively on the hypothalamus and pituitary. Stomach enteroendocrine cells Hypothalamus GHRH (+) and somatostatin (−) Anterior pituitary somatotrophs Liver IGF-1 synthesis Growth · tissue maintenance protein anabolism · lipolysis ↑ blood glucose (counter-insulin) ghrelin GHRH somatostatin GH (pulsatile) GH also acts directly on tissues IGF-1 IGF-1 + GH − − Somatostatin is the dominant brake. Sleep, exercise, and hypoglycaemia stimulate; high glucose suppresses.

Signaling chain

Section titled “Signaling chain”

GHRH (stimulatory) and somatostatin (inhibitory) from the hypothalamus jointly regulate GH release from anterior pituitary somatotrophs. GH acts directly on tissues and stimulates IGF-1 production, mainly by the liver. Ghrelin (from the stomach) also stimulates GH.

Function

Section titled “Function”

Drives linear growth in children and tissue maintenance/repair in adults. GH is anabolic for protein, lipolytic for fat, and diabetogenic (counter-regulatory to insulin — raises blood glucose). Most growth-promoting effects are mediated by IGF-1. Secretion is pulsatile, with the largest surge during slow-wave sleep.

Feedback

Section titled “Feedback”

IGF-1 and GH suppress GHRH and stimulate somatostatin. Somatostatin is the dominant brake. High glucose suppresses GH; hypoglycemia, exercise, and sleep stimulate it.

Clinical relevance

Section titled “Clinical relevance”
  • Excess — gigantism (before growth-plate fusion) or acromegaly (after); usually a pituitary adenoma.
  • Deficiency — short stature in children; reduced muscle mass, central adiposity, and poor quality of life in adults.
  • Because GH is pulsatile, a random level is uninformative — provocative/suppression testing is required.

Key labs

Section titled “Key labs”

IGF-1 (stable surrogate), oral glucose tolerance test (fails to suppress GH in acromegaly), GH stimulation tests (insulin tolerance, glucagon) for deficiency.