A peptide hormone of the gastrointestinal system responsible for stimulating the digestion of fat and protein.

CCK is synthesized and secreted by enteroendocrine cells in the duodenum.

CCK is synthesized and released by enteroendocrine cells in the mucosal lining of the small intestine, mostly in the duodenum and jejunum, called I cells, neurons of the enteric nervous system, and neurons in the brain.

Unlike secretin, which is an endocrine hormone, CCK actually works via stimulation of a neuronal circuit, the end-result of which is stimulation of the acinar cells to release their content. 

CCK also increases gallbladder contraction, resulting in bile squeezed into the cystic duct, common bile duct and eventually the duodenum. 

CCK stimulates production of the pancreatic zymogens.

Cholecystokinin (CCK) is gut peptide produced by the duodenum in response to fat and protiens. 

CCK has the effect of slowing gut motility and increasing satiety as well as activating release of pancreatic digestive enzymes and bile from the gallbladder.

Its presence causes the release of digestive enzymes and bile from the pancreas and gallbladder, respectively.

Acts as a hunger suppressant.

Gene location Chromosome 3.

Secreted by I-cells in the small intestine and induces contraction of the gallbladder, relaxes the sphincter of Oddi, reduces of gastric acid secretion, increases bile acid production in the liver, delays gastric emptying, and induces digestive enzyme production in the pancreas.

A member of the gastrin/cholecystokinin family of peptide hormones and is very similar in structure to gastrin.

Plays important physiologic roles both as a neuropeptide in the central nervous system and as a peptide hormone in the gut.

It participates digestion, satiety and anxiety.

It is released rapidly into the circulation in response to a meal.

The presence of fatty acids and/or certain amino acids in the chyme entering the duodenum, are the greatest stimulators of CCK

Its release is also stimulated by pancreatic acinar cell peptides, CCK-releasing protein by enterocytes in the gastric and intestinal mucosa, and acetylcholine released by the parasympathetic nerve fibers of the vagus nerve.

CCK has a relatively short half-life.

Mediates digestion in the small intestine by inhibiting gastric emptying.

It stimulates the acinar cells of the pancreas to release digestive enzymes, pancreozymin, that catalyze the digestion of fat, protein, and carbohydrates.

As the levels of the substances that stimulated the release of CCK drop, its concentration drops as well.

The release of CCK is inhibited by somatostatin and pancreatic peptide.

Trypsin, a protease released by pancreatic acinar cells, hydrolyzes CCK-releasing peptide and monitor peptide, in effect turning off the additional signals to secrete CCK.

CCK also causes the increased production of hepatic bile, stimulates the contraction of the gall bladder and the relaxation of the sphincter of Oddi, resulting in the delivery of bile into the duodenal part of the small intestine.

Bile salts form amphipathic lipids, micelles that emulsify fats, aiding in their digestion and absorption.

It mediates satiety by acting on the CCK receptors distributed widely throughout the central nervous system.

Its hunger suppression effect is related to the delay in gastric emptying time.

CCK stimulates the vagus nerve, the effects of which can be inhibited by capsaicin.

CCK stimulators effects oppose those of ghrelin, which has been shown to inhibit the vagus nerve.

It is found extensively throughout the central nervous system, with high concentrations found in the limbic system.

Elevated CCK levels causes increased anxiety by stimulating targets of basolateral amygdala, hippocampus, hypothalamus, peraqueductal grey, and cortical regions.

CCK has anxiety induvpcing effects with specific targets being the basolateral amygdala, hippocampus, hypothalamus, peraqueductal grey, and cortical regions.

The CCK tetrapeptide fragment CCK-4 causes anxiety and panic attacks.

It is implicated CCK as a cause of visual hallucinations in Parkinson’s disease.

It cannot cross the blood-brain barrier, but certain parts of the hypothalamus and brainstem are not protected by the barrier.

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