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Related Experiment Videos

Cholecystokinin and satiety: current perspectives.

T H Moran1

  • 1Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. tmoran@jhmi.edu

Nutrition (Burbank, Los Angeles County, Calif.)
|October 31, 2000
PubMed
Summary

Cholecystokinin (CCK) plays a key role in controlling meal size and body weight. Research shows CCK

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Area of Science:

  • Neuroscience
  • Endocrinology
  • Gastroenterology

Background:

  • The brain/gut peptide cholecystokinin (CCK) is known to inhibit food intake.
  • Research over the past 30 years has significantly advanced the understanding of CCK's role in ingestive behavior.

Purpose of the Study:

  • To investigate the physiological role of endogenous CCK in controlling meal size.
  • To explore the sites and mechanisms of CCK action in regulating food intake.
  • To examine the involvement of the CCK satiety pathway in mediating the effects of estradiol, insulin, and leptin on feeding.

Main Methods:

  • Utilizing the Otsuka Long Evans Tokushima Fatty (OLETF) rat model, which lacks CCK(A) receptors.
  • Investigating the impact of CCK receptor deficits on within-meals satiety signaling.

Main Results:

  • Demonstrated a physiological role for endogenous CCK in meal size control.
  • Identified sites and mechanisms of CCK action influencing food intake.
  • Uncovered roles for the CCK satiety pathway in modulating feeding behaviors influenced by estradiol, insulin, and leptin.

Conclusions:

  • Deficits in the CCK satiety signaling pathway can lead to long-term alterations in food intake and body weight.
  • The OLETF rat model provides a valuable tool for studying the consequences of impaired CCK signaling on ingestive behavior and metabolic regulation.

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