Decreased food intake in response to cholecystokinin (pancreozymin) in wild-type and obese mice (genotype ob/ob).

Cholecystokinin decreased food intake more effectively in obese mice than in wild-type mice. Following a 23-h fast and 10 min after an ip injection of 0, 30, 60 or 90 U/kg. CCK in physiological saline, eating, drinking and rearing rates were measured for a period of 20 min. Thirty units affected neither group, 60 U slowed the eating rate of obese mice significantly, and 90 U that of both groups, particularly the obese mice (P less than 0.001). Drinking and rearing rates remained unchanged. Obese mice were not hyperphagic under the conditions of the experiment and showed an increase in the latency period which preceded eating, compared with wild-type mice. The enhanced responsiveness to CCK, both in and out of the hyperphagic state, may be associated with low endogenous levels of satiety hormones in the obese mouse.