Title: Cholecystokinin
CAS Registry Number: 9011-97-6
Additional Names: Pancreozymin; cholecystokinin-pancreozymin; CCK-PZ
Literature References: Polypeptide hormone found in the mammalian gastrointestinal tract and brain. Stimulates pancreatic exocrine secretion and growth. May also play a role in appetite satiation, pain perception, and neuronal transmission. First shown to cause gallbladder contraction: Ivy, Oldberg, Am. J. Physiol. 86, 599 (1928). Discovery of a substance, designated as pancreozymin, which promotes secretion of digestive enzymes by the pancreas: Harper, Raper, J. Physiol. (London) 102, 115 (1943). Identity with pancreozymin: Jorpes et al., Acta Chem. Scand. 18, 2408 (1964). The C-terminal pentapeptide has been shown to be identical to that of gastrin and caerulein: V. Mutt, J. E. Jorpes, Eur. J. Biochem. 6, 156 (1968); eidem, Biochem. J. 125, 57P (1971). Various biologically active, amino-truncated forms have been identified. Cholecystokinin consisting of 33 amino acids (CCK-33) is the predominant gastrointestinal form; CCK-39 and CCK-58 have also been identified. CCK-8 is the predominant CNS form. Identification of CCK in brain: J. J. Vanderhaeghen et al., Nature 257, 604 (1975); G. J. Dockray, ibid. 264, 568 (1976). Distribution and molecular heterogeneity: J. F. Rehfeld, J. Biol. Chem. 253, 4022 (1978). Synthesis of the C-terminal dodecapeptide: M. A. Ondetti et al., J. Am. Chem. Soc. 92, 195 (1970). Synthesis of the N-terminal hexapeptide of porcine CCK-33: Bodanszky et al., J. Org. Chem. 37, 2303 (1972). Cloning and nucleotide sequence of the human cholecystokinin gene: Y. Takahashi et al., Proc. Natl. Acad. Sci. USA 82, 1931 (1985). Total synthesis of porcine CCK-33: Y. Kurano, Chem. Commun. 1987, 323; of human CCK-33: N. Fujii et al., ibid. 1988, 324. Proposed role in suppression of food intake: M. A. Della-Fera, C. A. Baile, Science 206, 471 (1979); C. J. Savory, M. J. Gentle, Experientia 36, 1191 (1980); M. A. Della-Fera et al., Science 212, 687 (1981); in regulation of hypothalamic peptides: S. Itoh et al., Life Sci. 25, 1725 (1979); in modulation of catecholaminergic activity: K. Fuxe et al., Eur. J. Pharmacol. 67, 329 (1980). There is also evidence that CCK acts as a specific antagonist of opiate analgesia: P. L. Faris et al., Science 219, 310 (1983). Reviews: E. Straus, R. S. Yalow, Fed. Proc. 38, 2320-2324 (1979); V. Mutt, Biochem. Soc. Trans. 8, 11-14 (1980); idem, Vitam. Horm. 39, 231-426 (1982). Review of physiology: G. J. Dockray, Br. Med. Bull. 38, 253-258 (1982); of role in appetite satiation and pain perception: G. Stacher, Psychoneuroendocrinology 11, 39-48 (1986). Symposium on neuronal CCK: Ann. N.Y. Acad. Sci. 448, 1-697 (1985).
Derivative Type: C-Terminal octapeptide see Sincalide
Cholestanol Cholesterol Cholestyramine Resin Cholic Acid Choline Alfoscerate

Symbols CCK (; MGC117187)
External IDs OMIM: 118440 MGI: 88297 HomoloGene: 583 ChEMBL: 1649050 GeneCards: CCK Gene
RNA expression pattern
PBB GE CCK 205827 at tn.png
More reference expression data
Species Human Mouse
Entrez 885 12424
Ensembl ENSG00000187094 ENSMUSG00000032532
UniProt P06307 P09240
RefSeq (mRNA) NM_000729 NM_031161
RefSeq (protein) NP_000720 NP_112438
Location (UCSC) Chr 3:
42.3 – 42.31 Mb
Chr 9:
121.49 – 121.5 Mb
PubMed search [1] [2]
CCK identified at bottom right.

Cholecystokinin (CCK or CCK-PZ; 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 synthesized 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.[1][2]