Gastrointestinal hormones !

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Exam priority: high

The gut makes its own hormones: they report what food arrived and tune acid, enzymes, bile, emptying and appetite.

Updated 2026-11-01

Also called: Gut peptides, Digestive hormones

See it in 3D: Stomach · Duodenum · Jejunum · Ileum · Pancreas · Gallbladder

Key points

Gastrin (G cells of the antrum): stimulated by peptides, distension and the vagus (via GRP); inhibited by acid (pH < 3) through somatostatin. Raises acid and is trophic to the mucosa.
Cholecystokinin, CCK (I cells of duodenum and jejunum): triggered by fat and amino acids; contracts the gallbladder, relaxes the sphincter of Oddi, drives pancreatic enzymes and slows gastric emptying.
Secretin (S cells of the duodenum): triggered by acid in the duodenum; calls for bicarbonate from the pancreas and bile ducts and suppresses gastrin.
GIP (K cells) and GLP-1 (L cells) are incretins: that is why oral glucose releases more insulin than the same glucose given IV.
Motilin: during fasting, every 90–120 min, it triggers the migrating motor complex (the between-meal 'housekeeper').
Classic trap: a gastrinoma (Zollinger–Ellison) gives multiple or distal ulcers and a high gastrin that does NOT fall with acid; secretin paradoxically raises it.

What it is

Endocrine cells scattered through the gastric and intestinal mucosa sense what is in the lumen and release hormones into the blood. Each one answers a specific signal (protein, fat, acid, glucose or fasting) and coordinates distant organs. Knowing who makes it, what triggers it and what it does answers most GI exam questions.

Key facts

There are three signalling routes: endocrine (gastrin, CCK, secretin, GIP, motilin), paracrine (somatostatin, histamine) and neurocrine (VIP, GRP, nitric oxide, substance P).
Gastrin and CCK share the same C-terminal end, so CCK is a weak agonist at the gastrin receptor.
VIP is a relaxing, secretory neurotransmitter; a tumour that makes it (VIPoma) causes watery diarrhea, hypokalemia and achlorhydria.

Gut hormones: source, trigger and actions

Hormone	Cell and site	Main trigger	Key actions
Gastrin	G cells, gastric antrum and duodenum	Peptides and amino acids, distension, vagus (GRP); inhibited by pH < 3	↑ HCl (via ECL-cell histamine), ↑ growth of gastric mucosa
CCK	I cells, duodenum and jejunum	Fatty acids and monoglycerides, amino acids	Gallbladder contraction, Oddi relaxation, ↑ pancreatic enzymes, ↓ gastric emptying, satiety
Secretin	S cells, duodenum	Acid in the duodenum (pH < 4.5), fatty acids	↑ pancreatic and biliary HCO₃⁻, ↓ gastrin and acid, ↓ emptying
GIP	K cells, duodenum and jejunum	Glucose, fat and amino acids	↑ glucose-dependent insulin (incretin), ↓ acid at high pharmacological levels
GLP-1	L cells, ileum and colon	Nutrients reaching the ileum	↑ insulin, ↓ glucagon, ↓ gastric emptying, satiety
Motilin	M cells, duodenum and jejunum	Fasting (cyclic release)	Starts the migrating motor complex
Somatostatin	D cells, stomach, gut and islets	Luminal acid; the 'brake' signal	Inhibits almost everything: gastrin, acid, enzymes, insulin, glucagon
Ghrelin	Gastric fundus cells	Fasting, empty stomach	↑ appetite (hypothalamus), ↑ growth hormone

Clinical notes

Gastrinoma: acid hypersecretion, refractory jejunal ulcers and diarrhea because lipase is inactivated in an over-acid duodenum.
Autoimmune atrophic gastritis or long-term proton pump inhibitor use: little acid → gastrin rises because the brake is gone (secondary hypergastrinemia).
Incretins are the physiological basis for GLP-1 analogues in type 2 diabetes and obesity.

Test yourself

Think of the answer, then tap the question to see it.

Why does oral glucose cause more insulin secretion than the same amount given intravenously?

Passing through the gut releases GIP (K cells) and GLP-1 (L cells), the incretins, which amplify glucose-dependent insulin secretion.

A patient with multiple ulcers has very high gastrin and a gastric pH of 1. What diagnosis fits and why is gastrin not suppressed?

Gastrinoma (Zollinger–Ellison). Tumour gastrin escapes the somatostatin brake that acid normally triggers, so it stays high despite the low pH.

Which hormone rises when a fatty meal reaches the duodenum, and what does it do to the gallbladder and stomach?

CCK. It contracts the gallbladder, relaxes the sphincter of Oddi, stimulates pancreatic enzymes and slows gastric emptying to give digestion time.

What stimulus releases secretin, and what secretion does it produce from the pancreas?

Acid entering the duodenum (pH below about 4.5). Secretin makes pancreatic duct cells secrete a bicarbonate-rich fluid that neutralizes chyme.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

In Biochemistry

← All of physiology

Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 23.2 Digestive System Processes and Regulation (OpenStax (Rice University), 2022); 23.4 The Stomach (OpenStax (Rice University), 2022); 23.6 Accessory Organs in Digestion: The Liver, Pancreas, and Gallbladder (OpenStax (Rice University), 2022); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 65). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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