The renin-angiotensin-aldosterone system and glucose homeostasis.

Luther JM, Brown NJ
Trends Pharmacol Sci. 2011 32 (12): 734-9

PMID: 21880378 · PMCID: PMC3223326 · DOI:10.1016/j.tips.2011.07.006

The renin-angiotensin-aldosterone system (RAAS) is inappropriately activated in obesity. In individuals at risk for diabetes, RAAS inhibition protects against kidney and heart disease, and also reduces the incidence of diabetes in large clinical trials. At a cellular level, angiotensin II (Ang II) and aldosterone induce insulin resistance by increasing oxidative stress and altering insulin signaling, leading to decreased glucose transport. Ang II also contributes to oxidative stress, inflammation, and apoptosis in pancreatic β cells. Aldosterone diminishes glucose-stimulated insulin secretion in vivo and in vitro from isolated pancreatic islets and cultured β cells through a mineralocorticoid receptor (MR)-independent mechanism. We review these findings in the context of pharmacological strategies interrupting the RAAS to highlight the potential application of these strategies to the prevention of diabetes progression.

Copyright © 2011 Elsevier Ltd. All rights reserved.

MeSH Terms (11)

Angiotensin-Converting Enzyme Inhibitors Angiotensin II Type 1 Receptor Blockers Animals Diabetes Mellitus Glucose Metabolism Disorders Humans Insulin-Secreting Cells Insulin Resistance Molecular Targeted Therapy Obesity Renin-Angiotensin System

Connections (2)

This publication is referenced by other Labnodes entities:

Links