Gastrin, secretin, cholecystokinin and GIP, each with a distinct trigger
Mnemonic
Four hormones, each with a stimulus and a job:
| Hormone | Source | Stimulus | Action |
|---|---|---|---|
| Gastrin | G cells, antrum | Peptides, gastric distension, vagus | Acid secretion |
| Secretin | S cells, duodenum | Acid in the duodenum | Bicarbonate from pancreas, inhibits gastrin |
| Cholecystokinin | I cells, duodenum | Fat and protein | Gallbladder contraction, pancreatic enzymes, satiety |
| GIP | K cells | Glucose, fat | Insulin release, the incretin effect |
“Secretin for acid, CCK for fat, gastrin for protein, GIP for glucose” links each to its trigger.
Secretin was the first hormone ever described, by Bayliss and Starling in 1902, and it is the physiological brake on gastrin, which is why a duodenum full of acid shuts the stomach down.
Somatostatin from D cells inhibits essentially everything, which is the basis of using octreotide in variceal bleeding and neuroendocrine tumours.
Expansion
| Hormone | Source | Stimulus | Main actions |
|---|---|---|---|
| Gastrin | G cells, antrum | Peptides, gastric distension, vagus | Acid secretion, mucosal growth |
| Secretin | S cells, duodenum | Acid in the duodenum | Pancreatic bicarbonate, inhibits gastrin |
| Cholecystokinin | I cells, duodenum | Fat and protein | Gallbladder contraction, pancreatic enzymes, sphincter of Oddi relaxation, satiety |
| Gastric inhibitory peptide (GIP) | K cells, duodenum | Glucose and fat | Insulin release, inhibits acid |
| Motilin | M cells | Fasting, cyclical | Migrating motor complex |
| Somatostatin | D cells | Acid | Inhibits nearly everything |
| VIP | Enteric neurones | Smooth muscle relaxation, intestinal secretion |
The organising idea is that each hormone answers the problem created by its stimulus: acid in the duodenum calls for bicarbonate, fat calls for bile and lipase, and glucose calls for insulin.
GIP is the basis of the incretin effect: oral glucose provokes far more insulin than the same amount given intravenously, which is exploited by GLP-1 agonists and DPP-4 inhibitors.