Cholecystokinin (CCK)
Also known as: CCK, pancreozymin
A peptide from I cells of the duodenum and jejunum, released by fat and protein digestion products, that contracts the gallbladder, relaxes the sphincter of Oddi, stimulates pancreatic enzyme secretion, slows gastric emptying and signals satiety.
Overview
I cells release CCK in several lengths (CCK-8, -33, -58) when long-chain fatty acids (≥≈12 carbons), monoglycerides, peptides and amino acids reach the duodenum. It acts mainly through CCK1 (CCK-A) receptors (Gq) — directly on gallbladder smooth muscle and, in humans, largely via vagal afferents that trigger reflex pancreatic acinar secretion.
Its actions coordinate fat digestion: gallbladder contraction and relaxation of the sphincter of Oddi deliver bile into the duodenum; pancreatic acinar cells release digestive enzymes (it potentiates secretin's bicarbonate effect); gastric emptying slows, matching delivery to digestive capacity; and vagal–brainstem signalling produces satiety and meal termination. CCK is also trophic to the exocrine pancreas.
- Location
Source: I cells of the duodenal and jejunal mucosa (also enteric and central neurons). Targets: gallbladder, sphincter of Oddi, pancreatic acini, stomach, vagal afferents.
Function
- Contracts the gallbladder and relaxes the sphincter of Oddi.
- Stimulates pancreatic enzyme secretion.
- Slows gastric emptying.
- Induces satiety.
- Physiology
Class: peptide (shares C-terminal pentapeptide with gastrin). Receptors: CCK1/CCK-A (Gq) — gallbladder, pancreas, vagus; CCK2/CCK-B in brain and stomach.
- Regulation
Stimulated by luminal fatty acids, monoglycerides, amino acids and peptides; released less when trypsin in the lumen degrades CCK-releasing peptides (feedback).
Clinical significance
Biliary colic after fatty meals
CCK-driven gallbladder contraction against a stone impacted in the cystic duct or Hartmann pouch causes post-prandial right upper quadrant pain. CCK (sincalide) is used in hepatobiliary scintigraphy to measure gallbladder ejection fraction.
Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.