Five rhesus monkeys were infused intravenously with partially purified cholecystokinin (CCK) just prior to a test meal of solid food after overnight food deprivation; CCK produced large, rapid, dose related suppressions of feeding. The lowest dose tested (5 Ivy U/kg body wt) produced a significant inhibition of food intake (26% suppression, P<0.05). Equivalent infusions of partially purified CCK or the synthetic COOH terminal octapeptide of CCK (a pure fragment with all the biological activity of the full molecule) produced equivalent suppressions. In a second experiment, gastric preloads of a potent releaser of endogenous CCK, L phenylalanine (L Phe) and a weak releaser, D phenylalanine (D Phe) were compared for their relative abilities to suppress food intake at a test meal in nine rhesus monkeys after overnight deprivation. L Phenylalanine produced large, rapid, dose related suppressions of feeding, but D Phe did not. The threshold dose of L Phe was 0.5 g/kg (32% suppression, P<0.01). Neither CCK nor L Phe caused signs of illness in these experiments. The results demonstrate that intravenous exogenous CCK suppresses feeding in rhesus monkeys and suggest that endogenous CCK has the same effect; they are consistent with the hypothesis that CCK is a satiety signal.
|Original language||English (US)|
|Number of pages||4|
|Journal||American Journal of Physiology|
|State||Published - Dec 1 1976|
ASJC Scopus subject areas
- Physiology (medical)