Cholecystokinin: a putative satiety signal.

The intestinal hormone cholecystokinin (CCK) elicits satiety in rats and inhibits food intake in rhesus monkeys. This behavioral effect is specifically related to the C-terminal octapeptide structure of CCK and is a new biological effect of the hormone. Endogenous CCK released by food entering the duodenum may inhibit feeding and elicit satiety under physiological conditions, but no experimental evidence is availabe on this point. Until such evidence becomes available, we believe that CCK should be considered a putative satiety signal. The satiety effect of CCK suggests a therapeutic role of CCK for human hyperphagia and obesity. An interesting therapeutic alternative to administration of exogenous CCK is the release of endogenous CCK by nutrients such as amino acids. These nutrients can be ingested as preloads which are calorically trivial, but which release significant amounts of CCK. Such preloads inhibit food intake in rhesus monkeys. Their efficacy in man has not been determined.