Abstract
Lee et al. report that an angiotensin II type 1 receptor blocker (ARB) improved glucose intolerance in OLETF rats, an experimental model of type 2 diabetes. ARB treatment resulted in modulation of the adipose tissue, leading to an increased number of small, differentiated adipocytes able to produce more adiponectin and less monocyte chemoattractant protein-1 and plasminogen activator inhibitor-1. This supports the relevance of the functional interplay between adipose tissue and the renin-angiotensin system in states of insulin resistance.
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