CorpusHuman Anatomy
EndocrineHormone

Gastrin

Also known as: G-17, G-34

A peptide from G cells of the gastric antrum that stimulates gastric acid secretion (mainly via histamine release from ECL cells) and growth of the gastric mucosa; acid in the antrum switches it off.

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Overview

ClassPeptide
ReceptorCCK2 — Gq
SourceAntral G cells

G cells of the pyloric antrum (and duodenum) release gastrin into the blood mainly as G-17 (antral) and G-34 in response to peptides and amino acids in the lumen, gastric distension and vagal stimulation via gastrin-releasing peptide. It acts on CCK2 (CCK-B) receptors (Gq), chiefly on enterochromaffin-like (ECL) cells, which release histamine that stimulates parietal cells via H2 receptors; it also acts directly on parietal cells. Gastrin is trophic to the oxyntic mucosa and ECL cells and increases gastric motility.

Negative feedback: when antral pH falls below ≈3, D cells release somatostatin, which inhibits G cells — the main brake on acid secretion. Secretin and GIP also inhibit gastrin release.

Location

Source: G cells of the gastric antrum and duodenum. Targets: ECL cells and parietal cells of the gastric body/fundus.

Function

  • Stimulates gastric acid secretion (via histamine and directly).
  • Trophic effect on gastric mucosa.
  • Increases gastric motility.
Physiology

Class: peptide (G-17, G-34). Receptor: CCK2/CCK-B — Gq.

Regulation

Stimulated by peptides/amino acids, distension, vagal GRP, high antral pH; inhibited by antral acid (pH <3, via somatostatin), secretin and GIP.

Clinical significance

Zollinger–Ellison syndrome (gastrinoma)

Gastrin-secreting neuroendocrine tumour (duodenum or pancreas, within the "gastrinoma triangle"; ≈25 % with MEN1): severe, multiple or distal (jejunal) peptic ulcers, diarrhoea and steatorrhoea (acid inactivates lipase), very high fasting gastrin despite low gastric pH; secretin stimulation paradoxically increases gastrin.

Hypergastrinaemia with low acid

Achlorhydria (autoimmune atrophic gastritis/pernicious anaemia) and long-term proton pump inhibitors raise gastrin through loss of acid feedback, causing ECL-cell hyperplasia and occasionally gastric carcinoid tumours.

Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.