image: Nlrp3 and IL-1 β in disease pathogenesis. Key metabolic imbalances attributable to increased adiposity—hyperlipidemia and hyperglycemia—activate Nlrp3 and, thus, IL-1β. In atherosclerosis, this accelerates lesion formation in which cholesterol crystallizes in macrophages and activates the inflammasome, which can promote plaque rupture. In T2D, insulin resistance further elevates blood glucose concentrations and signals for increased insulin and IAPP production. Excess IAPP can form oligomers that activate the inflammasome in islet macrophages, probably leading to β cell death and disease progression. This image relates to a Perspective that appeared in the May 4, 2011, issue of Science Translational Medicine, published by AAAS. The Perspective, by Dr. Seth Masters of Trinity College Dublin in Dublin, Ireland and colleagues, was titled, "The Inflammasome in Atherosclerosis and Type 2 Diabetes." view more
Credit: Image: C. Bickel/<i>Science</i> © 2011 AAAS