Anorectic effect of fenfluramine, cholecystokinin and neurotensin in genetically obese (ob/ob) mice.
To investigate the satiety defect of hyperphagic genetically obese (ob/ob) mice, acute feeding responses to three differently acting anorectic agents were determined in 7-9 weeks old lean (+/+) and ob/ob mice habituated to a restricted (0900-1230 hr) daily feeding routine. Fenfluramine (10 mg/kg), cholecystokinin (100 U/kg) and neurotensin (500 micrograms/kg), administered intraperitoneally 15 min before feeding, each produced a rapid but transient suppression of food consumption in ob/ob mice, similar to lean controls. The results suggest that neural satiety mechanisms triggered via serotoninergic pathways (fenfluramine), vagal afferents (cholecystokinin) and the hypothalamic paraventricular nucleus (neurotensin) are functional in ob/ob mice, supporting the view that the satiety defect of ob/ob mice resides outside of the nervous system.
D000818:Animals; D001067:Appetite Depressants; D002766:Cholecystokinin / Q000494:pharmacology*; D005247:Feeding Behavior / Q000187:drug effects; D005277:Fenfluramine / Q000494:pharmacology*; D006185:Habituation, Psychophysiologic; D006579:Heterozygote; D051379:Mice; D008820:Mice, Obese; D009496:Neurotensin / Q000494:pharmacology*; D012527:Satiation / Q000187:drug effects*; D013045:Species Specificity
D001067:Appetite Depressants; D005277:Fenfluramine; D009496:Neurotensin; D002766:Cholecystokinin