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Gene Review

CCK  -  cholecystokinin

Sus scrofa

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Disease relevance of CCK

  • We now report that no change was detected in either body weight or total daily food consumption at any time point during 2 weeks of intraperitoneally (i.p.) infused CCK [1].
  • These results demonstrate that endogenous levels of CCK regulate growth of this human cholangiocarcinoma [2].
  • 5. When cells were pre-incubated for 3 h in the presence of 200 ng/ml of pertussis toxin, the contraction induced by galanin was abolished while the CCK-induced contraction remained unchanged [3].
  • Action of cholecystokinin octapeptide and CCK-related peptides on neurons in inferior mesenteric ganglion of guinea pig [4].
  • At a suboptimal dose for pancreatic enzyme secretion (25 pmol/kg/h), CCK was found to potentiate the severity of the ensuing pancreatitis in both models [5].

Psychiatry related information on CCK


High impact information on CCK

  • Specific CCK binding sites have been demonstrated in the rat, guinea pig and human brain [10].
  • Cholecystokinin (CCK) is a neuropeptide present in the mammalian central nervous system (CNS) [10].
  • In microelectrode experiments acetylcholine (ACh), gastrin-cholecystokinin (CCK) as well as bombesin peptides evoked Ca2+-dependent opening of the K+ conductance pathway, resulting in membrane hyperpolarization [11].
  • We chose the Alzet constant infusion osmotic minipump to investigate possible alterations in body weight and food intake during continuous infusion of CCK [1].
  • Reductions in food intake and related exploratory behaviours are initiated by CCK at its peripheral receptor in the gut, which appears to transmit sensory feedback via the vagus nerve to brain regions mediating appetitive behaviours [1].

Chemical compound and disease context of CCK

  • Pancreatic weight, DNA, RNA, protein, and amylase content per 100 g body weight and secretory responses to CCK, carbamylcholine, and phorbol ester were determined at birth and 4 days in animals receiving MK329 in utero and were measured at 4 and 15 days in neonatally infused animals [12].
  • Moreover, our results on gallbladders from gallstone patients show that lorglumide is a highly effective antagonist of CCK-induced contractions despite the presence of chronic cholecystitis [13].
  • Pertussis toxin (200 ng/ml for 3 h) reversed the inhibitory effects of SS and baclofen on CCK-stimulated contraction and release [14].
  • In the presence of atropine naloxone elicited small contractures when added after peptides with primarily neural actions, including corticotropin-releasing factor, neurotensin and cholecystokinin octapeptide 26-33 sulfated form [15].
  • NSAIDs, at concentrations that inhibit naloxone-induced contractions, did not depress the maximal contracture to cholecystokinin and prostaglandin E1, but inhibited the submaximal one [16].

Biological context of CCK

  • Linkage analysis revealed that the CCK gene is located on porcine chromosome 13 [17].
  • Individuals from the European pig gene mapping project (PiGMaP) consortium reference families (eight full-sib families, 91 total progeny) were genotype to determine linkage relationships between the CCK gene and previously mapped loci [17].
  • CCK has been proposed as a satiety signal, inducing the behavioural sequence of satiety, or as an aversive internal stimulus, which inhibits food intake by inducing malaise [1].
  • Contraction induced by 10 nmol/L CCK was inhibited as follows: L 365,260 half maximal inhibition (IC50) = 1 nmol/L greater than L 364,718 (IC50 = 90 nmol/L) greater than proglumide (IC50 = 1 mumol/L) [18].
  • Incubation of acinar cells with CCK-33 at cell density of 0.2-0.3 mg acinar protein per ml resulted in stimulation of amylase release concomitant with significant and time-dependent decrease of the immunoreactive CCK [19].

Anatomical context of CCK

  • We further report that about 60% of the CCK in posterior lobe originates in cell bodies in the paraventricular nucleus of the hypothalamus [20].
  • RESULTS: More hydrophobic bile salts, such as TDC (as low as 5 micromol/L), concentration-dependently depressed (P < 0.05) both CCK- and field stimulation-induced gallbladder contractions [21].
  • Smooth muscle cells were dispersed from pig ileum circular muscle layer and incubated in the presence of various concentrations of CCK agonists and antagonists [18].
  • These results show that the CCK receptor of pig ileum smooth muscle cells is closely similar to the B receptor and is not dependent on an influx of extracellular Ca2+ to induce cell contraction [18].
  • Compounds I and II were competitive inhibitors of [3H]Boc[Ahx28,31]CCK-(27-33) binding to central CCK receptors and showed a high degree of selectivity for these binding sites (compound I: Ki for pancreas/Ki for brain, 179; compound II: Ki for pancreas/Ki for brain, 1979) [22].

Associations of CCK with chemical compounds

  • The CCK content of posterior pituitary is dramatically decreased by physiological perturbations which stimulate vasopressin or oxytocin release [20].
  • The inhibitory effect was also specific for certain agonists such as CCK (the action of which was partially mediated by cholinergic nerves, being depressed by atropine and abolished by tetrodotoxin), field stimulation, and nicotine [23].
  • EC50 for CCK tetrapeptide (CCK-4) was the same than for pentagastrin (30 pmol/L), which were more potent than CCK-8 (100 pmol/L) and unsulfated gastrin 17 (100 pmol/L), which in turn were more potent than unsulfated CCK heptapeptide (CCK-7; 300 pmol/L) and sulfated gastrin II (300 pmol/L) [18].
  • Dose-response curves to known agonists cholecystokinin (CCK), bethanechol, and KCl were constructed alone and in the presence of atropine (10(-6) mol/L), tetrodotoxin (10(-6) mol/L), and different bile salts, namely, taurodeoxycholate, tauroursodeoxycholate, taurocholate, glycodeoxycholate, and glycoursodeoxycholate [23].
  • Both brain and gut contain CCK octapeptide (CCK8) and an NH2-terminal fragment that is likely to be desoctapeptide-CCK33 [24].

Physical interactions of CCK


Regulatory relationships of CCK

  • 4. Vasoactive intestinal polypeptide (VIP) and isoprenaline, known to induce cell relaxation through an increase in intracellular cAMP level, inhibited CCK-induced cell contraction at concentrations ranging from 1 pM to 1 microM but failed to inhibit cell contraction induced by galanin [3].
  • Pretreatment with NADPH oxidase inhibitor PH2I, xanthine oxidase inhibitor allopurinol, and free-radical scavenger catalase also prevented TCDC-induced contraction and its inhibition of the CCK-induced contraction [26].
  • CONCLUSION: CCK inhibits gastrin secretion independently of paracrine somatostatin secretion [27].
  • However, both PYY and NPY concentration-dependently inhibited contraction induced by CCK-8 [25].
  • The CCK-A receptor antagonist L-364,718 was 300-fold more potent than the CCK-B receptor antagonist L-365,260 at inhibiting CCK-8-induced contraction [25].

Other interactions of CCK

  • CONCLUSIONS: In dogs, postprandial pancreatic secretion is controlled by a negative feedback mechanism mediated mainly by the release of secretin, but not by CCK [28].
  • On the contrary, 10 microM forskolin abolished the contraction induced by 10 nM CCK but had no effect on galanin-induced contraction [3].
  • These tetrapeptides elicit full agonist responses in stimulating pancreatic amylase release that are effectively blocked by a selective CCK-A receptor antagonist [29].
  • Plasma CCK levels were lower as a result of the MCT treatment compared with the saline and LCT treatments [30].
  • A double-labeling immunofluorescence technique stained 3 types of trigeminal cells and ocular nerve fibers: some immunoreactive for both peptides, some immunoreactive only for CCK and some immunoreactive only for SP [31].

Analytical, diagnostic and therapeutic context of CCK


  1. Rapid development of tolerance to the behavioural actions of cholecystokinin. Crawley, J.N., Beinfeld, M.C. Nature (1983) [Pubmed]
  2. Endogenous cholecystokinin regulates growth of human cholangiocarcinoma. Evers, B.M., Gomez, G., Townsend, C.M., Rajaraman, S., Thompson, J.C. Ann. Surg. (1989) [Pubmed]
  3. Intracellular pathways triggered by galanin to induce contraction of pig ileum smooth muscle cells. Botella, A., Delvaux, M., Bueno, L., Frexinos, J. J. Physiol. (Lond.) (1992) [Pubmed]
  4. Action of cholecystokinin octapeptide and CCK-related peptides on neurons in inferior mesenteric ganglion of guinea pig. Schumann, M.A., Kreulen, D.L. J. Pharmacol. Exp. Ther. (1986) [Pubmed]
  5. Cholecystokinin augmentation of 'surgical' pancreatitis. Benefits of receptor blockade. Modlin, I.M., Bilchik, A.J., Zucker, K.A., Adrian, T.E., Sussman, J., Graham, S.M. Archives of surgery (Chicago, Ill. : 1960) (1989) [Pubmed]
  6. Calcitonin gene-related peptide inhibits gallbladder contractility. Hashimoto, T., Poston, G.J., Greeley, G.H., Thompson, J.C. Surgery (1988) [Pubmed]
  7. The role of central and peripheral cholecystokinin in mediating appetitive behaviors. Crawley, J.N., Rojas-Ramirez, J.A., Mendelson, W.B. Peptides (1982) [Pubmed]
  8. Central nervous system cholecystokinin and the control of feeding behavior in sheep. Della-Fera, M.A., Baile, C.A. Prog. Clin. Biol. Res. (1985) [Pubmed]
  9. Cholecystokinin and satiation. Lieverse, R.J., Jansen, J.B., Lamers, C.B. The Netherlands journal of medicine. (1993) [Pubmed]
  10. Benzodiazepines antagonize cholecystokinin-induced activation of rat hippocampal neurones. Bradwejn, J., de Montigny, C. Nature (1984) [Pubmed]
  11. Quantification of Ca2+-activated K+ channels under hormonal control in pig pancreas acinar cells. Maruyama, Y., Petersen, O.H., Flanagan, P., Pearson, G.T. Nature (1983) [Pubmed]
  12. On the importance of cholecystokinin in neonatal pancreatic growth and secretory development in guinea pigs. Herrington, M.K., Joekel, C.S., Vanderhoof, J.A., Adrian, T.E. Pancreas (1995) [Pubmed]
  13. The effect of a novel CCK-antagonist (lorglumide) on human and guinea pig gallbladder strips: a tensiometric study. Portincasa, P., Brandonisio, R., Di Ciaula, A., Maggi, V., Chiloiro, M., Palasciano, G. Boll. Soc. Ital. Biol. Sper. (1990) [Pubmed]
  14. GABA mediation of the dual effects of somatostatin on guinea pig ileal myenteric cholinergic transmission. Roberts, D.J., Hasler, W.L., Owyang, C. Am. J. Physiol. (1993) [Pubmed]
  15. Neural activation of opioid mechanisms in guinea pig ileum by excitatory peptides. Garzón, J., Höllt, V., Sánchez-Blázquez, P., Herz, A. J. Pharmacol. Exp. Ther. (1987) [Pubmed]
  16. Effect of nonsteroidal anti-inflammatory drugs on withdrawal responses in guinea pig ileum after a brief exposure to morphine. Valeri, P., Morrone, L.A., Romanelli, L., Amico, M.C. J. Pharmacol. Exp. Ther. (1993) [Pubmed]
  17. Polymerase chain reaction-based polymorphisms in the porcine cholecystokinin (CCK) gene and assignment to chromosome 13. Clutter, A.C., Sasaki, S., Pomp, D. Anim. Genet. (1996) [Pubmed]
  18. Cholecystokinin and gastrin induce cell contraction in pig ileum by interacting with different receptor subtypes. Botella, A., Delvaux, M., Berry, P., Frexinos, J., Bueno, L. Gastroenterology (1992) [Pubmed]
  19. Characterization of interactions between CCK-33 and CCK receptors in isolated dispersed pancreatic acini. Hosotani, R., Chowdhury, P., Doi, R., Rayford, P.L. J. Cell. Physiol. (1992) [Pubmed]
  20. Cholecystokinin octapeptide in the rat hypothalamo-neurohypophysial system. Beinfeld, M.C., Meyer, D.K., Brownstein, M.J. Nature (1980) [Pubmed]
  21. Inhibitory effect of bile salts on gallbladder smooth muscle contractility in the guinea pig in vitro. Xu, Q.W., Freedman, S.M., Shaffer, E.A. Gastroenterology (1997) [Pubmed]
  22. Cyclic cholecystokinin analogues with high selectivity for central receptors. Charpentier, B., Pelaprat, D., Durieux, C., Dor, A., Reibaud, M., Blanchard, J.C., Roques, B.P. Proc. Natl. Acad. Sci. U.S.A. (1988) [Pubmed]
  23. The influence of bile salts on small intestinal motility in the guinea pig in vitro. Xu, Q., Shaffer, E.A. Gastroenterology (1992) [Pubmed]
  24. Post-translational processing of cholecystokinin in pig brain and gut. Eng, J., Shiina, Y., Straus, E., Yalow, R.S. Proc. Natl. Acad. Sci. U.S.A. (1982) [Pubmed]
  25. Functional CCK-A and Y2 receptors in guinea pig esophagus. Huang, S.C. Regul. Pept. (2000) [Pubmed]
  26. Effects of bile acids on the muscle functions of guinea pig gallbladder. Xiao, Z.L., Rho, A.K., Biancani, P., Behar, J. Am. J. Physiol. Gastrointest. Liver Physiol. (2002) [Pubmed]
  27. Cholecystokinin inhibits gastrin secretion independently of paracrine somatostatin secretion in the pig. Schmidt, P.T., Hansen, L., Hilsted, L., Holst, J.J. Scand. J. Gastroenterol. (2004) [Pubmed]
  28. Role of secretin in negative feedback regulation of postprandial pancreatic secretion in dogs. Imamura, M., Lee, K.Y., Song, Y., Moriyasu, M., Chang, T.M., Chey, W.Y. Gastroenterology (1993) [Pubmed]
  29. Boc-CCK-4 derivatives containing side-chain ureas as potent and selective CCK-a receptor agonists. Shiosaki, K., Lin, C.W., Kopecka, H., Tufano, M.D., Bianchi, B.R., Miller, T.R., Witte, D.G., Nadzan, A.M. J. Med. Chem. (1991) [Pubmed]
  30. Fats infused intraduodenally affect the postprandial secretion of the exocrine pancreas and the plasma concentration of cholecystokinin but not of peptide YY in growing pigs. Jakob, S., Mosenthin, R., Zabielski, R., Rippe, C., Winzell, M.S., Gacsalyi, U., Laubitz, D., Grzesiuk, E., Pierzynowski, S.G. J. Nutr. (2000) [Pubmed]
  31. Cholecystokinin-like immunoreactivity occurs in ocular sensory neurons and partially co-localizes with substance P. Kuwayama, Y., Stone, R.A. Brain Res. (1986) [Pubmed]
  32. Isolation of a large cholecystokinin precursor from canine brain. Eysselein, V.E., Reeve, J.R., Shively, J.E., Miller, C., Walsh, J.H. Proc. Natl. Acad. Sci. U.S.A. (1984) [Pubmed]
  33. Autoradiographic localization of cholecystokinin receptors in rodent brain. Zarbin, M.A., Innis, R.B., Wamsley, J.K., Snyder, S.H., Kuhar, M.J. J. Neurosci. (1983) [Pubmed]
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