Related Experiment Videos
Cholecystokinin: a putative satiety signal
Pharmacology, Biochemistry, and Behavior
|January 1, 1975
Summary
Cholecystokinin (CCK), an intestinal hormone, signals satiety and reduces food intake. Releasing CCK with nutrients may offer a therapeutic strategy for obesity and hyperphagia.
Area of Science:
- Neuroscience
- Gastroenterology
- Endocrinology
Background:
- The intestinal hormone cholecystokinin (CCK) is known to affect satiety.
- Its C-terminal octapeptide structure is crucial for this behavioral effect.
- The role of endogenous CCK in physiological feeding inhibition is not yet experimentally confirmed.
Purpose of the Study:
- To investigate the role of CCK as a satiety signal.
- To explore the therapeutic potential of CCK for hyperphagia and obesity.
- To evaluate nutrient-induced CCK release as a method to inhibit food intake.
Main Methods:
- Behavioral studies in rats and rhesus monkeys.
- Administration of exogenous CCK and nutrient preloads.
- Observation of food intake and satiety responses.
Main Results:
- CCK administration elicited satiety in rats and inhibited food intake in rhesus monkeys.
- Nutrient preloads that stimulate CCK release also inhibited food intake in rhesus monkeys.
- The C-terminal octapeptide of CCK was identified as the key structure for its satiety effect.
Conclusions:
- CCK is a putative satiety signal with potential therapeutic applications for obesity.
- Stimulating endogenous CCK release via nutrient preloads is a promising strategy to control food intake.
- Further research is needed to confirm the efficacy of CCK and nutrient preloads in humans.