Fifty Shades of Brown

The relationship between increased body mass index and risk for diabetes mellitus or cardiovascular disease is well established. Such observations have driven considerable interest into the nature of adipose tissue and what mechanisms might help explain how adipose tissue and specific aspects of adipocyte biology influence cardiometabolic disorders. For example, adipocytes are now recognized as a source of mediators released into the circulation, like the adipokines resistin and adiponectin, which can modulate inflammation, insulin sensitivity, and atherosclerosis. Other molecules released from adipocytes like free fatty acids and reactive oxygen species can also exert both local and distant effects that may be integral to the development of diabetes mellitus, atherosclerosis, and their complications. To an increasing extent, adipose tissue is now understood as an organ playing important physiological and pathological roles. Both the absence of fat, as with certain lipodystrophies, and excess adiposity are associated with diabetes mellitus, with mechanisms that appear to include infiltration of inflammatory cells into adipose tissue and the release of systemic mediators. Article see p 1067 To these and the many other adipocyte actions that continue to be uncovered, recent work has added another critical dimension to our evolving view of fat: the specific location of a given adipose depot. Subcutaneous white fat, visceral white fat, brown fat, epicardial fat, and perivascular fat—including fat around the coronaries, the thoracic aorta, and the abdominal aorta—have all been identified as distinct depots that exert unique local and systemic effects (Table). These issues are of particular interest given studies. suggesting that brown adipose tissue (BAT), which drives thermogenesis, is variably present in humans, associated with decreased adiposity, and may be a therapeutic target. In this issue of Circulation , Chang and colleagues add to this still emerging picture by providing the intriguing observation that a deficiency of peroxisome proliferator-activated …