| First Author | Takahashi N | Year | 2007 |
| Journal | Cell Metab | Volume | 6 |
| Issue | 6 | Pages | 506-12 |
| PubMed ID | 18054319 | Mgi Jnum | J:130439 |
| Mgi Id | MGI:3771678 | Doi | 10.1016/j.cmet.2007.10.011 |
| Citation | Takahashi N, et al. (2007) Increased energy expenditure, dietary fat wasting, and resistance to diet-induced obesity in mice lacking renin. Cell Metab 6(6):506-12 |
| abstractText | 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. |
