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- W2020104198 abstract "Hypothalamic noradrenergic mechanisms contribute to altered caloric intake in genetically obese (C57BL/6J, ob/ob) mice. Noradrenergic mechanisms, principally in the paraventricular hypothalamus and of the α2 subtype, have also been implicated in the macronutrient intake regulation of nonpathological models. Accordingly, this study assessed the extent to which clonidine, an α2 agonist, altered macronutrient intake in genetically obese (ob/ob) and lean (C57BL/6J +/?) mice. Following adaptation to a 6-h feeding regimen, mice were injected intraperitoneally with either clonidine (0.1, 0.5 mg/kg) or 0.15 M NaCl (Experiment 1) or 0.025 mg/kg clonidine or saline (Experiment 2) 30 min prior to simultaneous access to separate sources of carbohydrate, fat, and protein. Clonidine doses of 0.1 mg/kg or greater reduced total energy intake and intake of carbohydrate and fat (p<0.005) in all mice (Experiment 1). However, 0.025 mg/kg clonidine selectively increased ingestion of carbohydrate in obese mice by 212% of vehicle-injected values (p<0.001) without altering intake in lean mice (Experiment 2). These results implicate an α2 receptor mechanism in genetic obesity." @default.
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- W2020104198 date "1981-04-01" @default.
- W2020104198 modified "2023-09-25" @default.
- W2020104198 title "Cholecystokinin receptors are increased in cerebral cortex of genetically obese rodents" @default.
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- W2020104198 doi "https://doi.org/10.1016/0014-2999(81)90374-5" @default.
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