title: Epicardial steatosis, insulin resistance, and coronary artery disease.
abstract: Insulin resistance (IR) is the accepted primary cause of the metabolic syndrome. Visceral obesity is inversely correlated with insulin sensitivity. Hyperinsulinemia (a surrogate for IR) is highly prevalent in patients with coronary artery disease (CAD). Abnormalities in lipid metabolism give rise to steatosis in multiple organs. Evidence is rapidly accumulating to show that epicardial steatosis and expansion of coronary fat pad volume are highly deleterious and associated with increased risk for CAD. This article explores such associations from biochemical and structural standpoints, focusing on changes in epicardial adiposity.
authors.affiliation: CGH Medical Center, 101 East Miller Road, Sterling, IL 61081, USA. peter.toth@cghmc.com
authors.forename: Peter P
authors.initials: PP
authors.lastname: Toth
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism / Q000473:pathology; D003324:Coronary Artery Disease / Q000378:metabolism / Q000473:pathology*; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D005227:Fatty Acids / Q000378:metabolism; D006321:Heart; D006331:Heart Diseases / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D007333:Insulin Resistance; D050356:Lipid Metabolism; D024821:Metabolic Syndrome / Q000378:metabolism / Q000473:pathology; D010496:Pericardium / Q000378:metabolism / Q000473:pathology*; D012306:Risk
chemical_list: D005227:Fatty Acids