Cholecystokinin and satiety in rats and rhesus monkeys

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Abstract
When ingested food does not accumulate in the stomach or enter the small intestine, rats do not stop eating. Small amounts of food placed in the small intestine or intraperitoneal injections of the intestinal hormone cholecystokinin (CCK) elicit the full behavioral display of satiety in these sham-feeding rats. In rhesus monkeys, intravenous infusions of CCK produce large, dose-related reductions in meal size. In addition, gastric preloads of calorically trivial amounts of l-phenylalanine, but not d-phenylalanine, produce large reductions in meal size, suggesting that: 1) endogenous CCK acts as a “satiety signal,” and 2) certain foods may be very efficient releasers of such a satiety signal. Whether the satiety effect of CCK is physiological in rats and monkeys or operates in humans has not been determined.

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