Figure 1.

Thermogenic/oxidative potential of epicardial adipose tissue. We propose that epicardial adipocyte dysfunction occurs as a result of dietary, metabolic and environmental factors, which contribute to the loss of its brite adipocytes and progression of CAD in humans. Thermogenic activation of brite adipocytes, thus, represents a plausible target to alter the metabolic health of epicardial adipose tissue. However, regulation of the their oxidative and thermogenic capacity by well-known central and peripheral regulators such as SNS, FGF21 and NPs remains unknown. SNS, sympathetic nervous system; FGF21, fibroblast growth factor 21; NPs, natriuretic peptides; CAD, coronary artery disease.