Gastrin and Gastric Regulation
Gastrin is the principal hormone that stimulates the stomach to secrete acid. Released by G cells in the gastric antrum in response to a meal, it drives the parietal cells of the stomach to produce hydrochloric acid, both directly and by way of histamine, and helps coordinate gastric secretion and growth. Its release is tightly controlled by feedback so that acid is produced when food is present and switched off when the stomach empties.
Definition
Gastrin is a peptide hormone secreted by antral G cells that stimulates secretion of gastric acid by parietal cells, promotes the release of histamine from enterochromaffin-like cells, and contributes to the growth of the gastric mucosa; gastric regulation refers to the integrated neural and hormonal control of this secretion.
Scope
The topic covers where gastrin is made and what triggers its release, how it stimulates gastric acid secretion directly and through histamine, and the feedback loops (notably acid-induced somatostatin release) that regulate it. It is a physiology reference entry on the control of gastric secretion and does not provide clinical management advice.
Core questions
- What stimulates G cells to release gastrin during a meal?
- How does gastrin increase gastric acid secretion, directly and indirectly?
- How is acid secretion switched off when it is no longer needed?
- How do nerves and other hormones interact with gastrin to control the stomach?
Key concepts
- G cells of the gastric antrum
- Parietal cells and hydrochloric acid secretion
- Enterochromaffin-like cells and histamine
- Somatostatin (D-cell) negative feedback
- Cephalic, gastric, and intestinal phases
- Vagal stimulation of secretion
- Acid-mediated feedback inhibition
Mechanisms
Gastrin is released from antral G cells in response to a meal: peptides and amino acids in the lumen, gastric distension, and vagal stimulation all promote its secretion. Released into the blood, gastrin stimulates acid production in two ways: directly on parietal cells, and, importantly, by triggering enterochromaffin-like cells to release histamine, which then drives the parietal cell to secrete hydrochloric acid. The system is controlled by negative feedback: as luminal acidity rises, somatostatin from antral and oxyntic D cells inhibits both gastrin release and acid secretion, so that secretion is matched to the presence of food and is curtailed once the stomach is acidic or empty. Neural input, principally vagal, and other mediators integrate with this hormonal loop across the cephalic, gastric, and intestinal phases of digestion.
Clinical relevance
The gastrin–acid axis is fundamental to understanding gastric physiology and conditions involving acid secretion, and feedback by acidity on gastrin is a key concept in interpreting gastric function. This entry is reference physiology describing normal control and is not a basis for individual diagnosis or treatment.
History
John Edkins proposed in the early twentieth century that an antral extract he called gastrin stimulated gastric secretion, an idea that was disputed for decades because of confusion with histamine before gastrin was isolated and sequenced in the 1960s. Subsequent work mapped its release from G cells, its action through histamine and enterochromaffin-like cells, and its regulation by somatostatin, producing the integrated model of gastric acid control used today.
Key figures
- John Edkins
- Rod Dimaline
- Graham Dockray
- Mitchell Schubert
Related topics
Seminal works
- dockray-2001
- schubert-2008
Frequently asked questions
- What is the main job of gastrin?
- To stimulate the stomach to secrete acid in response to a meal, acting both directly on acid-producing parietal cells and indirectly by causing the release of histamine.
- How does the stomach stop secreting acid?
- Through negative feedback: as the stomach becomes acidic, somatostatin released from D cells inhibits gastrin release and acid secretion, switching the process off when food is no longer present.