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• W1991537701 abstract "Biochemical abnormalities in the hypothalamus of the genetically obese (C57B1/6J, ob/ob) mouse, including increased levels of endogenous norepinephrine (NE) in the paraventricular nucleus (PVN) and reduced medial hypothalamic NE metabolism, have been cited as evidence of a CNS defect contributing to altered caloric intake in this genetic strain. In the current study, the α2-antagonist yohimbine (YOH) and the α2-agonist clonidine (CLON) were administered systematically to 6-h meal-feeding obese and lean mice. Yohimbine (3–5 mg/kg, IP) significantly reduced total energy intake and intake of carbohydrate and fat, in both phenotypes, without altering protein intake. In contrast, CLON (25 μg/kg, IP) potentiated feeding, resulting in a shift in macronutrient selection toward a significant increase in the proportional intake of carbohydrate. Obese mice, however, showed an enhanced behavioral response to CLON injection. Pretreatment with 1 mg/kg YOH, a dose that alone did not significantly alter energy intake or diet selection, blocked CLON's stimulatory effect on feeding and carbohydrate preference. These results are consistent with a role for α2-noradrenergic receptors in appetite regulation of ob/ob and lean mice and suggest that disturbances in this system may be involved in the development of genetic obesity." @default.
• W1991537701 created "2016-06-24" @default.
• W1991537701 creator A5042939855 @default.
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• W1991537701 date "1992-12-01" @default.
• W1991537701 modified "2023-09-23" @default.
• W1991537701 title "Yohimbine attenuates clonidine-induced feeding and macronutrient selection in genetically obese (ob/ob) mice" @default.
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• W1991537701 doi "https://doi.org/10.1016/0091-3057(92)90478-x" @default.
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