cholecystokinin


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Related to cholecystokinin: enterogastrone, secretin

cho·le·cys·to·ki·nin

 (kō′lĭ-sĭs′tə-kī′nĭn)
n. Abbr. CCK
A hormone produced principally by the small intestine in response to the presence of fats, causing contraction of the gallbladder, release of bile, and secretion of pancreatic digestive enzymes. Also called pancreozymin.
American Heritage® Dictionary of the English Language, Fifth Edition. Copyright © 2016 by Houghton Mifflin Harcourt Publishing Company. Published by Houghton Mifflin Harcourt Publishing Company. All rights reserved.

cholecystokinin

(ˌkɒlɪˌsɪstəˈkaɪnɪn)
n
(Biochemistry) a hormone secreted by duodenal cells that stimulates the contraction of the gall bladder and secretion of pancreatic enzymes. Also called: pancreozymin
Collins English Dictionary – Complete and Unabridged, 12th Edition 2014 © HarperCollins Publishers 1991, 1994, 1998, 2000, 2003, 2006, 2007, 2009, 2011, 2014

cho•le•cys•to•ki•nin

(ˌkoʊ ləˌsɪs təˈkaɪ nɪn, ˌkɒl ə-)

n.
a hormone secreted by the upper intestine that stimulates contraction of the gallbladder and increases secretion of pancreatic juice. Abbr.: CCK
[1925–30]
Random House Kernerman Webster's College Dictionary, © 2010 K Dictionaries Ltd. Copyright 2005, 1997, 1991 by Random House, Inc. All rights reserved.

cholecystokinin

A hormone that causes the gallbladder to contract and so release bile into the duodenum.
Dictionary of Unfamiliar Words by Diagram Group Copyright © 2008 by Diagram Visual Information Limited
ThesaurusAntonymsRelated WordsSynonymsLegend:
Noun1.cholecystokinin - a gastrointestinal hormone that stimulates the secretion of pancreatic enzymes and the contraction and emptying of the gall bladder; its release is stimulated by the presence of fatty acids and amino acids in the small intestine
gastrointestinal hormone, GI hormones - hormones that affect gastrointestinal functioning
Based on WordNet 3.0, Farlex clipart collection. © 2003-2012 Princeton University, Farlex Inc.
References in periodicals archive ?
The overexpression of cholecystokinin receptor subtype 2 (CCK2R) is involved in various malignancies, such as medullary thyroid carcinoma (MTC), small cell lung cancer (SCLC), and neuroendocrine tumours (NET) [3,4] and therefore represents an interesting target for peptide receptor radionuclide imaging and therapy.
Magnocellular neurons of the PVN and supraoptic nucleus of the hypothalamus also produce a number of anorexigenic neuropeptides, including CART, pituitary adenylate cyclase-activating polypeptide, cholecystokinin (CCK), and nesfatin-1 (51), and are activated during feeding and by satiety peptides such as CCK and GLP1.
For example, the intake of fatty foods slows gastric emptying and causes a reduction in the basal pressure of the LES through a mechanism probably mediated by cholecystokinin (CCK) that can directly act on the LES, or indirectly, by inhibiting the action of gastrin [24].
Protein triggers cholecystokinin, a hormone that signals the brain to slow down the emptying of the stomach.
It also stimulates hormones secreted by gastrointestinal mucosa cells, such as gastrin, cholecystokinin, and glucagon.
Food contents in the duodenum will stimulate the release of cholecystokinin and causes contraction of gallbladder.
Cholecystokinin (CCK) is a peptide hormone secreted by the gastrointestinal tract, and its effects include gallbladder and pancreatic secretion, gastric and intestinal motor function, reduced food intake and stimulation of GH secretion (Canosa et al., 2007; Crespo et al., 2014; Micale et al., 2014; Dalmolin et al., 2015).
In addition, acidic environment of the gut stimulates the secretion of pepsin, gastrin and cholecystokinin, playing an essential role in the feed utilization, and subsequently improving growth performance (Hayat et al., 2014).
(9-11) In addition, there is evidence that NOD1 responses are key factors in the development of pancreatitis as reflected in the experimental pancreatitis caused by cholecystokinin hyperstimulation.
Their findings was published last week in Neuron under the title "(http://www.cell.com/neuron/fulltext/S0896-6273(17)30596-2?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627317305962%3Fshowall%3Dtrue) Initiation of Behavioral Response to Antidepressants by Cholecystokinin Neurons of the Dentate Gyrus ."
For example, cholecystokinin (CCK) analogues cause pancreatitis in rodents in the absence of alcohol treatments only at doses much greater than those needed to activate known physiologic responses such as pancreatic enzyme secretion and gallbladder contraction (Lam et al.