| First Author | Currie PJ | Year | 1992 |
| Journal | Pharmacol Biochem Behav | Volume | 43 |
| Issue | 4 | Pages | 1039-46 |
| PubMed ID | 1475285 | Mgi Jnum | J:12222 |
| Mgi Id | MGI:60472 | Doi | 10.1016/0091-3057(92)90478-x |
| Citation | Currie PJ, et al. (1992) Yohimbine attenuates clonidine-induced feeding and macronutrient selection in genetically obese (ob/ob) mice. Pharmacol Biochem Behav 43(4):1039-46 |
| abstractText | 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 alpha 2-antagonist yohimbine (YOH) and the alpha 2-agonist clonidine (CLON) were administered systemically 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 micrograms/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 alpha 2-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. |
