FIG. 1.
The ectopic adiposity phenotype. Ectopic fat accumulation in the abdominal cavity (visceral fat) and in organs like pericardium, liver, and pancreas (A), and muscle wasting/intramuscular fat accumulation (B) are bidirectionally linked to chronic inflammation (C) and insulin resistance (D), both of which have been linked to conventional and novel pathways of cardiometabolic risk.9 Ectopic fat is a major driver of atherosclerosis and its acute complications: epicardial fat (A1) has been linked to AF, accelerated coronary atherosclerosis, and left ventricular diastolic dysfunction20; hepatic fat (NAFLD) (A2) causally contributes to atherogenic dyslipidemia and is closely linked to subclinical atherosclerosis22; and pancreatic fat (A3) has been linked to beta-cell dysfunction23 and concomitant postprandial and fasting hyperglycemia. Chronically elevated serum glucose levels, and postprandial glucose spikes in particular, promote oxidative stress/chronic inflammation, endothelial dysfunction, and sympathetic hyperactivity, and result in the formation of AGEs. Glycation damage has been pathophysiologically linked to numerous chronic disease states such as cardiovascular aging.24 Down arrows indicate decreased levels, and up arrows indicate increased levels. AF, arrhythmia/atrial fibrillation; AGEs, advanced glycation end products; NAFLD, non-alcoholic fatty liver disease. Color images are available online.