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Increased energy expenditure, dietary fat wasting, and resistance to diet-induced obesity in mice lacking renin.


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.

SUBMITTER: Takahashi N 

PROVIDER: S-EPMC2174204 | biostudies-literature | 2007 Dec

REPOSITORIES: biostudies-literature

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Increased energy expenditure, dietary fat wasting, and resistance to diet-induced obesity in mice lacking renin.

Takahashi Nobuyuki N   Li Feng F   Hua Kunjie K   Deng Jianbei J   Wang Chih-Hong CH   Bowers Robert R RR   Bartness Timothy J TJ   Kim Hyung-Suk HS   Harp Joyce B JB  

Cell metabolism 20071201 6


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 di  ...[more]

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