ArticleFrontiers in endocrinology2012
Transgenic mice overexpressing Renin exhibit glucose intolerance and diet-genotype interactions.
Article in Frontiers in endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 15 citations in OpenAlex.
- Regulation and Functions of the Renin-Angiotensin System in White and Brown Adipose Tissue.Comprehensive Physiology · 2017Review
- Adipose tissue (P)RR regulates insulin sensitivity, fat mass and body weight.Molecular metabolism · 2016Article
- A novel mouse model of advanced diabetic kidney disease.PloS one · 2014Article
- Obesity-induced inflammation and insulin resistance.Frontiers in endocrinology · 2014Article
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Authors and funding
10 authors at 7 institutions in 3 countries.
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Abstract
Numerous animal and clinical investigations have pointed to a potential role of the renin-angiotensin system (RAS) in the development of insulin resistance and diabetes in conditions of expanded fat mass. However, the mechanisms underlying this association remain unclear. We used a transgenic mouse model overexpressing renin in the liver (RenTgMK) to examine the effects of chronic activation of RAS on adiposity and insulin sensitivity. Hepatic overexpression of renin resulted in constitutively elevated plasma angiotensin II (four- to six-fold increase vs. wild-type, WT). Surprisingly, RenTgMK mice developed glucose intolerance despite low levels of adiposity and insulinemia. The transgenics also had lower plasma triglyceride levels. Glucose intolerance in transgenic mice fed a low-fat diet was comparable to that observed in high-fat fed WT mice. These studies demonstrate that overexpression of renin and associated hyperangiotensinemia impair glucose tolerance in a diet-dependent manner and further support a consistent role of RAS in the pathogenesis of diabetes and insulin resistance, independent of changes in fat mass.
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