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Does interference with the renin-angiotensin system protect against diabetes? Evidence and mechanisms
N J van der Zijl1, C C M Moors, G H Goossens
1Diabetes Center, Department of Internal Medicine, VU University Medical Center, Amsterdam, The Netherlands. nj.vdzijl@vumc.nl
Abstract:
Agents interfering with the renin-angiotensin system (RAS) were consistently shown to lower the incidence of type 2 diabetes mellitus (T2DM), as compared to other antihypertensive drugs, in hypertensive high-risk populations. The mechanisms underlying this protective effect of RAS blockade using angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers on glucose metabolism are not fully understood. In this article, we will review the evidence from randomized controlled trials and discuss the proposed mechanisms as to how RAS interference may delay the onset of T2DM. In particular, as T2DM is characterized by β-cell dysfunction and obesity-related insulin resistance, we address the mechanisms that underlie RAS blockade-induced improvement in β-cell function and insulin sensitivity.
Insights
Agents blocking the renin-angiotensin system (RAS) reduce type 2 diabetes mellitus (T2DM) risk in hypertensive patients. This review explores how RAS blockade improves insulin sensitivity and beta-cell function, potentially delaying T2DM onset.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Metabolic Disorders
Background:
- Hypertensive high-risk populations show reduced type 2 diabetes mellitus (T2DM) incidence with renin-angiotensin system (RAS) interfering agents compared to other antihypertensives.
- Mechanisms for RAS blockade's protective effect on glucose metabolism are not fully elucidated.
- T2DM involves beta-cell dysfunction and insulin resistance, particularly in obesity.
Purpose of the Study:
- Review evidence from randomized controlled trials on RAS interference and T2DM.
- Discuss proposed mechanisms for how RAS blockade may delay T2DM onset.
- Address RAS blockade's impact on beta-cell function and insulin sensitivity.
Main Methods:
- Review of randomized controlled trials (RCTs).
- Discussion of proposed mechanistic pathways.
- Focus on beta-cell function and insulin sensitivity.
Main Results:
- RAS blockade demonstrates a protective effect against T2DM in hypertensive individuals.
- Proposed mechanisms involve improvements in beta-cell function.
- Proposed mechanisms involve improvements in insulin sensitivity.
Conclusions:
- RAS interference, via ACE inhibitors or ARBs, may delay T2DM development.
- Further research is needed to fully understand the mechanisms of RAS blockade on glucose metabolism.
- RAS blockade shows potential for managing T2DM risk in high-risk populations.
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