Abstract
1. 1. 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. 2. 2. Fenfluramine (10 mg/kg), cholecystokinin (100 U/kg) and neurotensin (500 μg/kg), administered intraperitoneally 15min before feeding, each produced a rapid but transient suppression of food consumption in ob/ob mice, similar to lean controls. 3. 3. 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.
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