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Feeding-suppressive mechanism of sulfated cholecystokinin (26-33) in chicks

Tetsuya Tachibana1, Kiyoko Matsuda, Motoko Kawamura

  • 1Department of Agrobiological Science, Faculty of Agriculture, Ehime University, Matsuyama 790-8566, Japan. tetsu@agr.ehime-u.ac.jp

Comparative Biochemistry and Physiology. Part A, Molecular & Integrative Physiology
|January 10, 2012
PubMed

Insights

Cholecystokinin (CCK) suppresses appetite in neonatal chicks, with sulfated CCK8S being most effective. This effect may involve stress pathways and requires specific molecular structures for activity.

Area of Science:

  • Neuroendocrinology
  • Animal Physiology
  • Gastrointestinal Hormones

Background:

  • Cholecystokinin (CCK) is known to reduce food intake in mammals.
  • Limited research exists on CCK's anorexigenic effects in neonatal chicks.

Purpose of the Study:

  • To investigate the mechanism of CCK's appetite-suppressing effect in neonatal chicks.
  • To determine the structural requirements for CCK's anorexigenic activity.
  • To explore the potential involvement of stress in CCK's effects.

Main Methods:

  • Administered various forms of CCK (sulfated CCK8S, non-sulfated CCK8, CCK4) via intraperitoneal (IP) and intracerebroventricular (ICV) routes.
  • Measured food intake following CCK administration.
  • Assessed conditioned aversion and plasma corticosterone levels.
  • Utilized astressin, a corticotropin-releasing hormone receptor antagonist, in co-injection studies.

Main Results:

  • Sulfated CCK8S significantly reduced food intake after both IP and ICV administration.
  • Non-sulfated CCK8 showed a weaker, dose-dependent anorexigenic effect, while CCK4 had no effect.
  • CCK8S administration led to conditioned aversion and increased corticosterone, suggesting a stress/malaise component.
  • Astressin partially attenuated the central anorexigenic effect of CCK8S.

Conclusions:

  • N-terminal amino acids and tyrosine sulfation are crucial for CCK8S's appetite-suppressing action in chicks.
  • The anorexigenic effect of central CCK8S may be mediated by stress and/or malaise pathways.

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