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Related Experiment Videos

Cholecystokinin-induced anorexia depends on serotoninergic function.

D Stallone1, S Nicolaïdis, J Gibbs

  • 1Centre National de la Recherche Scientifique, Collège de France, Paris.

The American Journal of Physiology
|May 1, 1989
PubMed
Summary

Cholecystokinin (CCK) reduces food intake, but this effect depends on the brain's serotonin system. Blocking serotonin receptors with metergoline reversed CCK's satiety effects in rats, indicating a crucial link.

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Area of Science:

  • Neuroscience
  • Gastroenterology
  • Pharmacology

Background:

  • Choleystokinin (CCK) is a gut hormone known to influence satiety.
  • The serotoninergic system (involving serotonin or 5-HT) plays a role in regulating appetite and mood.
  • Previous research suggests a potential interaction between CCK and serotonin pathways in appetite control.

Purpose of the Study:

  • To investigate the relationship between cholecystokinin (CCK)-induced satiety and the serotoninergic system.
  • To determine if blocking serotonin receptors affects CCK's ability to suppress food intake.

Main Methods:

  • Male rats were administered the COOH-terminal octapeptide of CCK (CCK-8) alone or with serotonin receptor blockers.
  • Metergoline (MET), a blocker active in the brain and periphery, and xylamidine tosylate (XYL), a peripheral blocker, were used.

Related Experiment Videos

  • Food intake was measured after CCK-8 administration in combination with or without receptor blockers.
  • Main Results:

    • CCK-8 significantly reduced food intake in a dose-dependent manner.
    • Both doses of metergoline (MET) attenuated CCK-8-induced satiety, restoring food intake to control levels.
    • Xylamidine tosylate (XYL) had no effect on CCK-8-induced satiety.
    • A high dose of MET alone increased food intake, while a lower dose did not.

    Conclusions:

    • The satiety effect of CCK-8 is dependent on the functioning of the serotoninergic system.
    • This interaction likely occurs at central nervous system sites.
    • Serotonin pathways are crucial mediators of CCK's inhibitory action on food intake.