Cholecystokinin inhibits food intake in genetically obese (C57BL/6j-ob) mice.
Cholecystokinin (CCK, 20% pure) inhibited liquid food intake in obese and lean male mice after 1.5 and 4.5 hr of food deprivation. CCK decreased meal size without changing the duration of the postprandial intermeal interval. The inhibition of food intake was relatively specific. The largest dose of CCK tested (40 U/kg) had no effect on water intake in lean mice and it merely changed the pattern of intake in obese mice. Obese mice were as sensitive as lean mice to the satiating effect of CCK after 1.5 hr and 4.5 hr of food deprivation. Since CCK decreased meal size in obese mice and since obese mice were normally sensitive to CCK, CCK could be the circulating satiety factor that Coleman [4] postulated was deficient in obese mice. The results, however, only indicate that CCK could be the deficient factor. Other experiments are required to prove the point.
D000818:Animals; D002766:Cholecystokinin / Q000494:pharmacology*; D005247:Feeding Behavior / Q000187:drug effects*; D005508:Food Deprivation / Q000502:physiology; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009765:Obesity / Q000503:physiopathology*
D002766:Cholecystokinin