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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

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 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.^[1][2]

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.

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

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.

As a neuropeptide, CCK mediates satiety by acting on the CCK receptors distributed widely throughout the central nervous system. In humans, CCK administration causes nausea and anxiety, and weakly decreases the desire to eat.^[3] The mechanism for this hunger suppression is thought to be a decrease in the rate of gastric emptying.^[4]

The effects of CCK vary between individuals. For example, in rats, CCK administration significantly reduces hunger in young males, but is less effective in older subjects, and even less effective in females. The hunger-suppressive effects of CCK also diminish in obese rats.^[5]

• Antianalgesia
• Proglumide

1. ^ Kissin I, Bright CA, Bradley EL Jr. Acute tolerance to continuously infused alfentanil: the role of cholecystokinin and N-methyl-D-aspartate-nitric oxide systems. Anesthesia and Analgesia. 2000 Jul;91(1):110-6.
2. ^ Fukazawa Y, Maeda T, Kiguchi N, Tohya K, Kimura M, Kishioka S. Activation of spinal cholecystokinin and neurokinin-1 receptors is associated with the attenuation of intrathecal morphine analgesia following electroacupuncture stimulation in rats. Journal of Pharmacological Sciences. 2007 Jun;104(2):159-66.
3. ^ Greenough A, Cole G, Lewis J, Lockton A, Blundell J (1998). "Untangling the effects of hunger, anxiety, and nausea on energy intake during intravenous cholecystokinin octapeptide (CCK-8) infusion". Physiol Behav 65 (2): 303-10. PMID 9855480. 
4. ^ Shillabeer G, Davison J (1987). "Proglumide, a cholecystokinin antagonist, increases gastric emptying in rats". Am J Physiol 252 (2 Pt 2): R353-60. PMID 3812772. 
5. ^ Fink H, Rex A, Voits M, Voigt J (1998). "Major biological actions of CCK--a critical evaluation of research findings". Exp Brain Res 123 (1-2): 77-83. PMID 9835394. 

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