The renin-angiotensin system may serve as a mechanistic link between obesity and insulin resistance, with evidence suggesting that RAS inhibition protects against the development of type-2 diabetes.
This review highlights the role of the renin-angiotensin system, particularly in adipose tissue, as a potential mechanistic link between obesity and insulin resistance.
The renin-angiotensin system (RAS) is classically known for its role in regulation of blood pressure, fluid and electrolyte balance. Recently, several local RASs in organs such as brain, heart, pancreas and adipose tissue have also been identified. Evidence from clinical trials suggests that in addition to anti-hypertensive effects, pharmacological inhibition of RAS also provides protection against the development of type-2 diabetes. Moreover, animal models with targeted inactivation of RAS genes exhibit improved insulin sensitivity and are protected from high-fat diet-induced obesity and insulin resistance. Because there is evidence for RAS overactivation in obesity, it is possible that RAS is a link between obesity and insulin resistance. This review summarizes the evidence and mechanistic insights on the associations between RAS, obesity and insulin resistance, with special emphasis on the role of adipose tissue RAS in the pathogenesis of metabolic derangements in obesity.
Kalupahana et al. (Mon,) conducted a review in Obesity and insulin resistance. Renin-angiotensin system (RAS) inhibition was evaluated. The renin-angiotensin system may serve as a mechanistic link between obesity and insulin resistance, with evidence suggesting that RAS inhibition protects against the development of type-2 diabetes.
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