Increased Energy Expenditure, Dietary Fat Wasting, and Resistance to Diet-Induced Obesity in Mice Lacking Renin

Nobuyuki Takahashi, Feng Li, Kunjie Hua, Jianbei Deng, Chih Hong Wang, Robert R. Bowers, Timothy J. Bartness, Hyung Suk Kim, Joyce B. Harp

Research output: Contribution to journalArticlepeer-review

80 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)506-512
Number of pages7
JournalCell Metabolism
Volume6
Issue number6
DOIs
Publication statusPublished - 2007 Dec 5
Externally publishedYes

Keywords

  • HUMDISEASE

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology

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