Ghrelin
Also known as: hunger hormone
An acylated 28-amino-acid peptide secreted mainly by the gastric fundus during fasting that stimulates appetite and growth hormone release — the only known circulating hunger hormone.
Overview
Ghrelin is made by X/A-like (P/D1) endocrine cells of the oxyntic mucosa of the gastric fundus and body, with smaller amounts from the duodenum, islet ε cells and the hypothalamus. To be active it must be acylated with octanoic acid on serine-3 by ghrelin O-acyltransferase (GOAT). Levels rise before meals and with fasting and fall rapidly after eating, particularly after carbohydrate.
It acts on the growth hormone secretagogue receptor (GHSR-1a), a Gq-coupled GPCR: in the arcuate nucleus it activates orexigenic NPY/AgRP neurons (and vagal afferents), stimulating hunger; at somatotrophs and the hypothalamus it stimulates GH release; it also increases gastric motility and acid secretion and promotes fat storage.
- Location
Source: X/A-like (P/D1) cells of the gastric fundus and body. Targets: arcuate nucleus, somatotrophs, vagal afferents, stomach.
Function
- Stimulates appetite and meal initiation.
- Stimulates GH secretion.
- Increases gastric motility and acid secretion; promotes adiposity.
- Physiology
Class: acylated peptide (28 aa). Receptor: GHSR-1a — Gq.
- Regulation
Rises with fasting, before meals and after weight loss; suppressed by food intake (especially carbohydrate), insulin and GH.
Clinical significance
Weight loss and bariatric surgery
Diet-induced weight loss raises ghrelin, contributing to hunger and weight regain; sleeve gastrectomy removes the fundus and lowers ghrelin, one reason it reduces appetite.
Prader–Willi syndrome
Very high ghrelin levels accompany the insatiable hyperphagia of this imprinting disorder (paternal 15q11–q13 deficiency).
Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.