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Increased energy expenditure, dietary fat wasting, and resistance to diet-induced obesity in mice lacking renin |
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| Authors: | Takahashi Nobuyuki Li Feng Hua Kunjie Deng Jianbei Wang Chih-Hong Bowers Robert R Bartness Timothy J Kim Hyung-Suk Harp Joyce B |
| Affiliation: | 1Department of Pathology and Laboratory Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA 2Department of Cell and Molecular Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA 3Department of Nutrition, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA 4Department of Biology, Neurobiology and Behavior Program, Center for Behavioral Neuroscience, Georgia State University, Atlanta, GA 30302, USA |
| Abstract: | An overactive renin-angiotensin system is associated with obesity and the metabolic syndrome. However, the mechanisms behind it are unclear. Cleaving angiotensinogen to angiotensin I by renin is a rate-limiting step of angiotensin II production, but renin is suggested to have angiotensin-independent effects. We generated mice lacking renin (Ren1c) using embryonic stem cells from C57BL/6 mice, a strain prone to diet-induced obesity. Ren1c−/− mice are lean, insulin sensitive, and resistant to diet-induced obesity without changes in food intake and physical activity. The lean phenotype is likely due to a higher metabolic rate and gastrointestinal loss of dietary fat. Most of the metabolic changes in Ren1c−/− mice were reversed by angiotensin II administration. These results support a role for angiotensin II in the pathogenesis of diet-induced obesity and insulin resistance. |
| Keywords: | HUMDISEASE |
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