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Publication : Diet-induced obese mice retain endogenous leptin action.

First Author  Ottaway N Year  2015
Journal  Cell Metab Volume  21
Issue  6 Pages  877-82
PubMed ID  25980347 Mgi Jnum  J:226133
Mgi Id  MGI:5695823 Doi  10.1016/j.cmet.2015.04.015
Citation  Ottaway N, et al. (2015) Diet-induced obese mice retain endogenous leptin action. Cell Metab 21(6):877-82
abstractText  Obesity is characterized by hyperleptinemia and decreased response to exogenous leptin. This has been widely attributed to the development of leptin resistance, a state of impaired leptin signaling proposed to contribute to the development and persistence of obesity. To directly determine endogenous leptin activity in obesity, we treated lean and obese mice with a leptin receptor antagonist. The antagonist increased feeding and body weight (BW) in lean mice, but not in obese models of leptin, leptin receptor, or melanocortin-4 receptor deficiency. In contrast, the antagonist increased feeding and BW comparably in lean and diet-induced obese (DIO) mice, an increase associated with decreased hypothalamic expression of Socs3, a primary target of leptin. These findings demonstrate that hyperleptinemic DIO mice retain leptin suppression of feeding comparable to lean mice and counter the view that resistance to endogenous leptin contributes to the persistence of DIO in mice.
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