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Gene Review

Cck  -  cholecystokinin

Mus musculus

Synonyms: CCK, Cholecystokinin
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Disease relevance of Cck

  • Cholecystokinin appears to play a contributory role in the development of pancreatitis [1].
  • Since CCK can function as a satiety factor when administered to rodents, localization of Cckbr near the tub mutation identifies this receptor as a possible candidate gene for this obesity mutation [2].
  • CCK-deficient mice are viable and fertile and exhibit normal body weight [3].
  • This result demonstrates that CCK is not required for protein-induced pancreatic hypertrophy and increased proteolytic enzyme content [3].
  • Finally, pertussis toxin inhibited the CCK-induced increase in the Ins-1,4,5-P3/PIP2 ratio in normal pancreatic islets [4].

Psychiatry related information on Cck

  • Leptin, injected intraperitoneally (i.p.) at low doses (4-120 microg/kg), which did not influence feeding behavior for the first 3 hr postinjection, decreased food intake dose dependently by 47-83% during the first hour when coinjected with a subthreshold dose of CCK [5].
  • These results demonstrate that centrally as well as peripherally administered CCK-8 suppresses locomotor activity in mice through an interaction with CCK-A, but not CCK-B, receptors [6].
  • Small intestinal CCK levels in psychological stress mice were significantly lower than those in the control group (0.75+/-0.53 microg/g vs 1.98+/-1.17 microg/g, P<0.01), whereas plasma CCK concentrations were not different between the groups [7].
  • Cholecystokinin-related peptides, after systemic or central administration, prevent carbon monoxide-induced amnesia in mice [8].
  • Influence of the selective cholecystokinin antagonist L-364,718 on pain threshold and morphine analgesia [9].

High impact information on Cck

  • Cells were significantly more sensitive to NAADP than to either cADPR or InsP3, whereas higher concentrations of NAADP selectively inactivated CCK-evoked Ca2+ signals in pancreatic acinar cells, indicating that NAADP may function as an intracellular messenger in mammalian cells [10].
  • Excitation of the non-cholinergic nerves stimulates amylase secretion by a different intracellular coupling mechanism from that activated by cholinergic nerves or by peptides belonging to the cholecystokinin, gastrin or bombesin families [11].
  • Straus and Yalow showed that brain CCK levels were reduced in the cerebral cortex of both genetically obese (ob/ob) and normal mice after a 2-5-day fast [12].
  • We show here that fasting in mice significantly increases CCK binding due to an increased number of CCK receptors in the olfactory bulb and hypothalamus, but not in other brain regions [12].
  • Cholecystokinin (CCK) is the parent molecule of a family of polypeptide hormones, some of which are secreted from the small intestine after food ingestion and stimulate both exocrine secretion and gall bladder contraction [12].

Chemical compound and disease context of Cck


Biological context of Cck


Anatomical context of Cck


Associations of Cck with chemical compounds

  • These results indicate the existence of a functional synergistic interaction between leptin and CCK leading to early suppression of food intake which involves CCK-A receptors and capsaicin-sensitive afferent fibers [5].
  • In contrast to amylase release, stimulation of acinar glucose transport by CCK or carbamylcholine was not augmented by VIP, secretin, IBMX or 8-Br-cyclic AMP [18].
  • VIP, IBMX and 8-Br-cyclic AMP, all of which act through or mimic the action of cyclic AMP, potentiated the secretory response to maximal concentrations of CCK, carbamylcholine and the ionophore A23187, all of which act via intracellular calcium [18].
  • The aim of this study was to investigate the effect of cholecystokinin (CCK) receptor antagonist on the abnormal behavior and dopamine (DA) transmission of tenascin (TN)-gene knockout mice [19].
  • L-364,718 and L-365,260 did not alter LPS-induced decrease in social investigation, whatever the route of administration, suggesting that endogenous cholecystokinin does not mediate the effect of proinflammatory cytokines on social exploration in mice [20].

Physical interactions of Cck

  • Studies of IGF II binding to acini at low temperature (15 degrees C) and binding to particulate fractions from acini were also consistent with the effect of insulin to increase and CCK8 to decrease the internalization of IGF II [21].
  • Collectively, these data suggest that CCK interacts at the CCKB receptor to inhibit tonically the release and/or availability of an endogenous substance acting at opioid delta receptors [22].
  • The results indicated galanin regulates CCK secretion by modulation of K+ ATP and cAMP production through receptors coupled to a PTX-sensitive G protein [23].

Co-localisations of Cck


Regulatory relationships of Cck


Other interactions of Cck


Analytical, diagnostic and therapeutic context of Cck


  1. Beneficial effects of cholecystokinin-receptor blockade and inhibition of proteolytic enzyme activity in experimental acute hemorrhagic pancreatitis in mice. Evidence for cholecystokinin as a major factor in the development of acute pancreatitis. Niederau, C., Liddle, R.A., Ferrell, L.D., Grendell, J.H. J. Clin. Invest. (1986) [Pubmed]
  2. Localization of the murine cholecystokinin A and B receptor genes. Samuelson, L.C., Isakoff, M.S., Lacourse, K.A. Mamm. Genome (1995) [Pubmed]
  3. Pancreatic function in CCK-deficient mice: adaptation to dietary protein does not require CCK. Lacourse, K.A., Swanberg, L.J., Gillespie, P.J., Rehfeld, J.F., Saunders, T.L., Samuelson, L.C. Am. J. Physiol. (1999) [Pubmed]
  4. Phosphoinositide metabolism in a polyoma-BK-virus-transformed pancreatic islet cell line: evidence for constitutively activated phospholipase C. Giaever, A.K., Haukland, H.H., Bertinussen, A., Vonen, B., Malm, D., Huseby, N.E., Florholmen, J. Int. J. Cancer (1993) [Pubmed]
  5. Synergistic interaction between leptin and cholecystokinin to reduce short-term food intake in lean mice. Barrachina, M.D., Martínez, V., Wang, L., Wei, J.Y., Taché, Y. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  6. Effects of CCK antagonists on CCK-induced suppression of locomotor activity in mice. Hirosue, Y., Inui, A., Miura, M., Nakajima, M., Okita, M., Himori, N., Baba, S., Kasuga, M. Peptides (1992) [Pubmed]
  7. Effects of psychological stress on small intestinal motility and expression of cholecystokinin and vasoactive intestinal polypeptide in plasma and small intestine in mice. Cao, S.G., Wu, W.C., Han, Z., Wang, M.Y. World J. Gastroenterol. (2005) [Pubmed]
  8. Cholecystokinin-related peptides, after systemic or central administration, prevent carbon monoxide-induced amnesia in mice. Maurice, T., Hiramatsu, M., Kameyama, T., Hasegawa, T., Nabeshima, T. J. Pharmacol. Exp. Ther. (1994) [Pubmed]
  9. Influence of the selective cholecystokinin antagonist L-364,718 on pain threshold and morphine analgesia. Poggioli, R., Vergoni, A.V., Sandrini, M., Barbafiera, L., Marrama, D., Bertolini, A. Pharmacology (1991) [Pubmed]
  10. Coordination of agonist-induced Ca2+-signalling patterns by NAADP in pancreatic acinar cells. Cancela, J.M., Churchill, G.C., Galione, A. Nature (1999) [Pubmed]
  11. Control of enzyme secretion by non-cholinergic, non-adrenergic nerves in guinea pig pancreas. Pearson, G.T., Davison, J.S., Collins, R.C., Petersen, O.H. Nature (1981) [Pubmed]
  12. Alterations in brain cholecystokinin receptors after fasting. Saito, A., Williams, J.A., Goldfine, I.D. Nature (1981) [Pubmed]
  13. Proglumide, a cholecystokinin receptor antagonist, exacerbates alloxan-induced diabetes mellitus in Swiss mice. Parmar, N.S., Tariq, M., Ageel, A.M. J. Pharm. Pharmacol. (1987) [Pubmed]
  14. Ciliary neurotrophic factor restores gallbladder contractility in leptin-resistant obese diabetic mice. Graewin, S.J., Kiely, J.M., Svatek, C.L., Pitt, H.A. J. Surg. Res. (2006) [Pubmed]
  15. Altered control of gastric acid secretion in gastrin-cholecystokinin double mutant mice. Chen, D., Zhao, C.M., Håkanson, R., Samuelson, L.C., Rehfeld, J.F., Friis-Hansen, L. Gastroenterology (2004) [Pubmed]
  16. Cholecystokinin levels in prohormone convertase 2 knock-out mouse brain regions reveal a complex phenotype of region-specific alterations. Beinfeld, M.C., Blum, A., Vishnuvardhan, D., Fanous, S., Marchand, J.E. J. Biol. Chem. (2005) [Pubmed]
  17. Cholecystokinin expression in the developing and regenerating pancreas and intestine. Liu, G., Pakala, S.V., Gu, D., Krahl, T., Mocnik, L., Sarvetnick, N. J. Endocrinol. (2001) [Pubmed]
  18. Interaction of cholecystokinin and vasoactive intestinal polypeptide on function of mouse pancreatic acini in vitro. Burnham, D.B., McChesney, D.J., Thurston, K.C., Williams, J.A. J. Physiol. (Lond.) (1984) [Pubmed]
  19. Effects of cholecystokinin-B receptor antagonist on dopamine system in tenascin mutant mice. Fukamauchi, F., Wang, Y.J., Mataga, N., Kusakabe, M. Neuroreport (1997) [Pubmed]
  20. Cholecystokinin receptors do not mediate the behavioral effects of lipopolysaccharide in mice. Bluthé, R.M., Michaud, B., Kelley, K.W., Dantzer, R. Physiol. Behav. (1997) [Pubmed]
  21. Effect of intracellular Ca2+ on insulin-like growth factor II. internalization into pancreatic acini. Roles of insulin and cholecystokinin. Mössner, J., Logsdon, C.D., Potau, N., Williams, J.A., Goldfine, I.D. J. Biol. Chem. (1984) [Pubmed]
  22. Enhancement of morphine antinociception by a CCKB antagonist in mice is mediated via opioid delta receptors. Vanderah, T.W., Bernstein, R.N., Yamamura, H.I., Hruby, V.J., Porreca, F. J. Pharmacol. Exp. Ther. (1996) [Pubmed]
  23. Galanin inhibits cholecystokinin secretion in STC-1 cells. Chang, C.H., Chey, W.Y., Coy, D.H., Chang, T.M. Biochem. Biophys. Res. Commun. (1995) [Pubmed]
  24. Reduced ghrelin, islet amyloid polypeptide, and peptide YY expression in the stomach of gastrin-cholecystokinin knockout mice. Friis-Hansen, L., Wierup, N., Rehfeld, J.F., Sundler, F. Endocrinology (2005) [Pubmed]
  25. Cholecystokinin-induced antinociception is not blocked by CCK-A or CCK-B receptor antagonists. Williams, C.L., Rosenfeld, G.C., Burks, T.F. Peptides (1997) [Pubmed]
  26. The effect of somatostatin analogue octreotide on amylase secretion from mouse pancreatic acini. Ishiguro, H., Hayakawa, T., Kondo, T., Shibata, T., Kitagawa, M., Sakai, Y., Sobajima, H., Nakae, Y., Tanikawa, M. Digestion (1993) [Pubmed]
  27. Levels of somatostatin and cholecystokinin in the brain of ataxic mutant mice. Matsui, K., Masui, A., Kato, N., Adachi, K. Life Sci. (1993) [Pubmed]
  28. Molecular cloning of the mouse CCK gene: expression in different brain regions and during cortical development. Vitale, M., Vashishtha, A., Linzer, E., Powell, D.J., Friedman, J.M. Nucleic Acids Res. (1991) [Pubmed]
  29. Immunohistochemical localization of substance P, vasoactive intestinal polypeptide and gastrin-releasing peptide in vas deferens and seminal vesicle, and the effect of these and eight other neuropeptides on resting tension and neurally evoked contractile activity. Stjernquist, M., Håkanson, R., Leander, S., Owman, C., Sundler, F., Uddman, R. Regul. Pept. (1983) [Pubmed]
  30. Adult carboxypeptidase E-deficient fat/fat mice have a near-total depletion of brain CCK 8 accompanied by a massive accumulation of glycine and arginine extended CCK: identification of CCK 8 Gly as the immediate precursor of CCK 8 in rodent brain. Wang, W., Cain, B.M., Beinfeld, M.C. Endocrine (1998) [Pubmed]
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