Cholecystokinin and Pancreatic Secretion

Cholecystokinin, usually abbreviated CCK, is a hormone released from the upper small intestine when fat and protein reach it. It stimulates the pancreas to secrete digestive enzymes and the gallbladder to contract and deliver bile, so that the chemistry of digestion matches the meal. It also slows gastric emptying and signals satiety, coordinating several digestive responses to a fatty, protein-rich meal.

Definition

Cholecystokinin is a peptide hormone released by enteroendocrine I cells of the duodenum and jejunum in response to luminal fat and protein, which stimulates secretion of digestive enzymes from the pancreatic acinar cells, causes contraction of the gallbladder with relaxation of the sphincter of Oddi, slows gastric emptying, and contributes to satiety.

Scope

The topic covers the release of cholecystokinin from intestinal I cells, its stimulation of pancreatic enzyme secretion and gallbladder contraction, its effects on gastric emptying and appetite, and how its actions complement those of secretin. It is a physiology reference entry and does not provide clinical management advice.

Core questions

• What in a meal triggers cholecystokinin release, and from which cells?
• How does cholecystokinin stimulate the pancreas and the gallbladder?
• How do cholecystokinin and secretin act together on the pancreas?
• How does cholecystokinin influence gastric emptying and appetite?

Key concepts

• I cells of the duodenum and jejunum
• Pancreatic acinar enzyme secretion
• Gallbladder contraction and the sphincter of Oddi
• CCK and secretin complementarity
• Slowing of gastric emptying
• Satiety signalling
• Vagal pathways in CCK action

Mechanisms

When the products of fat and protein digestion enter the duodenum and jejunum, enteroendocrine I cells release cholecystokinin into the blood. Cholecystokinin acts on pancreatic acinar cells to stimulate secretion of an enzyme-rich fluid, providing the lipases, proteases, and amylase needed for digestion, and it causes the gallbladder to contract while the sphincter of Oddi relaxes, delivering bile to emulsify fat. It complements secretin, which mainly stimulates a bicarbonate-rich fluid: together the two hormones match the volume, alkalinity, and enzyme content of pancreatic juice to the meal. Cholecystokinin also slows gastric emptying, giving the intestine time to process what it has received, and it acts on vagal afferents and central pathways to promote satiety. Much of its action involves vagal reflex pathways as well as direct hormonal effects.

Clinical relevance

Cholecystokinin physiology underlies the understanding of pancreatic and biliary function and of how meals are processed and appetite is regulated. This entry presents normal control mechanisms as reference knowledge and is not a basis for individual diagnosis or treatment.

History

Ivy and Oldberg described a hormone causing gallbladder contraction in 1928 and named it cholecystokinin; a separate factor stimulating pancreatic enzyme secretion was called pancreozymin, and the two were later shown to be the same peptide. Subsequent work characterised its molecular forms, its release from intestinal I cells in response to fat and protein, and its roles in pancreatic secretion, gallbladder emptying, gastric emptying, and satiety, establishing cholecystokinin as a central integrator of the intestinal phase of digestion.

Key figures

• Andrew Ivy
• Eric Oldberg
• Rodger Liddle
• Jens Rehfeld

Seminal works

• rehfeld-2017
• liddle-2000

Frequently asked questions

What does cholecystokinin do after a fatty meal?

It stimulates the pancreas to release digestive enzymes and the gallbladder to contract and deliver bile, while also slowing gastric emptying and promoting a feeling of fullness.

How do cholecystokinin and secretin work together?

Cholecystokinin mainly drives the enzyme-rich part of pancreatic secretion, while secretin drives the bicarbonate-rich, alkaline fluid; together they tailor pancreatic juice to neutralise acid and digest the meal.