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

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

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

    nobuyuki takahashiNobuyuki Takahashi,feng liFeng Li,kunjie huaKunjie Hua,jianbei dengJianbei Deng,chih-hong wangChih-Hong Wang,robert r bowersRobert R Bowers,timothy j bartnessTimothy J Bartness,hyung-suk kimHyung-Suk Kim,joyce b harpJoyce B Harp,nobuyuki takahashiNobuyuki Takahashi,feng liFeng Li,kunjie huaKunjie Hua,jianbei dengJianbei Deng,chih-hong wangChih-Hong Wang,robert r bowersRobert R Bowers,timothy j bartnessTimothy J Bartness,hyung-suk kimHyung-Suk Kim,joyce b harpJoyce B Harp,

    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.

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

    n takahashiN Takahashi,f liF Li,k huaK Hua,j dengJ Deng,ch wangCH Wang,rr bowersRR Bowers,tj bartnessTJ Bartness,hs kimHS Kim,jb harpJB Harp,n takahashiN Takahashi,f liF Li,k huaK Hua,j dengJ Deng,ch wangCH Wang,rr bowersRR Bowers,tj bartnessTJ Bartness,hs kimHS Kim,jb harpJB Harp,

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

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Cell metabolism

    VOLUME: 6

    Page Numbers: 506-12

    Journal Abbreviation: Cell Metab.

    ISSN: 1550-4131

    DAY: 6

    MONTH: Dec

    YEAR: 2007

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

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    LANGUAGE: eng

    NlmUniqueID: 101233170

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

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

    AFFILIATION: Department of Pathology and Laboratory Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. ntakaha@med.unc.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIDDK

    GRANT: P30DK56350

    ACRONYM: DK

    MEDLINETA: Cell Metab

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