Cholecystokinin

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Cholecystokinin
Identifiers
Symbol(s)	CCK; MGC117187
External IDs	OMIM: 118440 MGI: 88297 Homologene: 583
Gene ontology Molecular Function: • neuropeptide hormone activity Cellular Component: • extracellular region • soluble fraction • axon Biological Process: • neuron migration • signal transduction • axonogenesis • eating behavior
RNA expression pattern
More reference expression data
Orthologs
	Human	Mouse
Entrez	885	12424
Ensembl	ENSG00000187094	ENSMUSG00000032532
Uniprot	P06307	Q53WS9
Refseq	NM_000729 (mRNA) NP_000720 (protein)	NM_031161 (mRNA) NP_112438 (protein)
Location	Chr 3: 42.27 - 42.28 Mb	Chr 9: 121.34 - 121.34 Mb
Pubmed search	[2]	[3]

CCK identified at bottom right.
Cholecystokinin
Identifiers
Symbol	CCK
Entrez	885
HUGO	1569
OMIM	118440
RefSeq	NM_000729
UniProt	P06307
Other data
Locus	Chr. 3 pter-p21

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Cholecystokinin (CCK; from Greek chole, "bile"; cysto, "sac"; kinin, "move"; hence, move the bile-sac (gallbladder)) is a peptide hormone of the gastrointestinal system responsible for stimulating the digestion of fat and protein. Cholecystokinin, previously called pancreozymin, is synthesised by I-cells in the mucosal epithelium of the small intestine and secreted in the duodenum, the first segment of the small intestine, and causes the release of digestive enzymes and bile from the pancreas and gallbladder, respectively. It also acts as a hunger suppressant. Recent evidence has suggested that it also plays a major role in inducing drug tolerance to opioids like morphine and heroin, and is partly implicated in experiences of pain hypersensitivity during opioid withdrawal.

Structure

CCK is composed of varying numbers of amino acids (e.g., CCK58, CCK33, CCK8) depending on post-translational modification of the CCK gene product, preprocholecystokinin. CCK is very similar in structure to gastrin, another of the gastrointestinal hormones, so much so that the last five C-terminal amino acids are same as those of gastrin. CCK58 comprises a helix-turn-helix configuration.

Release and Function

CCK mediates a number of physiological processes, including digestion and satiety.

Digestion

Secretion of CCK by the duodenal and intestinal mucosa is stimulated by fat- or protein-rich chyme entering the duodenum. It then inhibits gastric emptying and gastric acid secretion and mediates digestion in the duodenum. It acts on the pancreas to stimulate the secretion of a juice rich in pancreatic digestive enzymes. Together these enzymes catalyze the digestion of fat, protein, and carbohydrates. Thus the levels of the substances which stimulated the release of CCK drop and the concentration of the hormone drops as well. The release of CCK is also inhibited by somatostatin.

CCK also causes the increased production of hepatic bile, and stimulates the contraction of the gallbladder and the relaxation of the Sphincter of Oddi (Glisson's sphincter), resulting in the delivery of bile into the duodenal part of the small intestine. Bile salts form amphipathic micelles that emulsify fats, aiding in their digestion and absorption.

Neurobiology

As a neuropeptide, CCK mediates satiety by acting on the CCK receptors distributed widely throughout the central nervous system. In humans, it has been suggested that CCK administration causes nausea and anxiety, and weakly decreases the desire to eat is the reason for CCK administration to induce a satiating effect. Some studies have given a strong correlation for the satiating effect, but have not proven or disproven that CCK administration causes nauseau or anxiety Benoit et al (2003). The mechanism for this hunger suppression is thought to be a decrease in the rate of gastric emptying.

The effects of CCK vary between individuals. For example, in rats, CCK administration significantly reduces hunger in young males, but is slightly less effective in older subjects, and even slightly less effective in females. The hunger-suppressive effects of CCK also are reduced in obese rats.

See also

• Antianalgesia
• Cholecystokinin antagonist
• Proglumide

External links

• MeSH Cholecystokinin
• Physiology at MCG 6/6ch2/s6ch2_14

de:Cholecystokininit:Colecistochinina