Cholecystokinin suppresses food intake by inhibiting gastric emptying.

In a search for the physiological mechanisms that could mediate and characterize a satiety function for the hormone cholecystokinin (CCK), we examined in Macaca mulatta the effect of intraperitoneal injections (0.1-0.8 microgram/kg) and intravenous infusions (60-240 ng.kg-1.h-1) of the C-terminal octapeptide of CCK on gastric emptying of saline test meals. Within these dose ranges, gastric emptying was inhibited by this hormone to a degree comparable with that produced by intraintestinal nutrient. The onset of the inhibition is rapid and its effect brief. At the doses of CCK that produce gastric inhibition, CCK would not affect feeding in a fasted monkey unless the stomach was filled with saline. This result suggests that a satiety influence of circulating CCK is an indirect one. The satiety effect depends upon inhibition of gastric emptying, which then leads to gastric distention with further food injection. CCK thus can be considered a link in a chain of physiological elements producing the short-term satiety that leads to the appropriate interruption of a meal or bout of feeding behavior.