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• W2009790701 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." @default.
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• W2009790701 date "2007-12-01" @default.
• W2009790701 modified "2023-10-18" @default.
• W2009790701 title "Increased Energy Expenditure, Dietary Fat Wasting, and Resistance to Diet-Induced Obesity in Mice Lacking Renin" @default.
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• W2009790701 doi "https://doi.org/10.1016/j.cmet.2007.10.011" @default.
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