Secretin
A 27-amino-acid peptide from duodenal S cells, released when acid enters the duodenum, that stimulates bicarbonate-rich pancreatic and biliary secretion and inhibits gastric acid — "nature's antacid" and the first hormone ever discovered.
Overview
Secretin was discovered by Bayliss and Starling in 1902, giving rise to the word "hormone". S cells in the duodenal (and upper jejunal) mucosa release it when chyme lowers duodenal pH below ≈4.5 (fatty acids also contribute). Acting through the secretin receptor (Gs/cAMP), it stimulates pancreatic duct cells to secrete a large volume of HCO₃⁻-rich fluid via the CFTR chloride channel and apical Cl⁻/HCO₃⁻ exchange, and stimulates bicarbonate secretion by cholangiocytes and Brunner glands. The bicarbonate neutralises gastric acid, protecting the duodenal mucosa and providing the near-neutral pH at which pancreatic enzymes work.
It also inhibits gastrin release and gastric acid secretion, slows gastric emptying and potentiates the action of CCK on the pancreas.
- Location
Source: S cells of the duodenal and proximal jejunal mucosa. Targets: pancreatic duct cells, bile duct epithelium, stomach.
Function
- Stimulates pancreatic and biliary bicarbonate secretion.
- Inhibits gastric acid secretion and gastrin release.
- Slows gastric emptying.
- Physiology
Class: peptide (27 aa; glucagon family). Receptor: secretin receptor — Gs/cAMP.
- Regulation
Released by duodenal acid (pH <≈4.5) and fatty acids; secretion falls once acid is neutralised.
Clinical significance
Secretin tests
In Zollinger–Ellison syndrome, IV secretin paradoxically increases gastrin (gastrinoma cells express secretin receptors). Secretin-enhanced MRCP improves visualisation of pancreatic ducts; the secretin stimulation test assesses exocrine pancreatic function.
Cystic fibrosis
Defective CFTR prevents secretin-driven bicarbonate and fluid secretion, so viscous secretions block pancreatic ducts, causing exocrine pancreatic insufficiency.
Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.