Central obesity as a clinical marker of adiposopathy; increased visceral adiposity as a surrogate marker for global fat dysfunction

PURPOSE OF REVIEW Subcutaneous adipose tissue (SAT) is often described as 'protective'. Visceral adipose tissue (VAT) is often described as 'pathologic'. However, both SAT and VAT have protective and pathologic potential, with interdependent biologic functions. RECENT FINDINGS Most of the body's (excess) energy is stored as fat in SAT. If during positive caloric balance, SAT does not undergo adequate adipogenesis, then excess energy may result in adipocyte hypertrophy, leading to hypoxia, immunopathies, and endocrinopathies. Energy overflow may promote accumulation of pericardial fat, perivascular fat, and myocardial fat, which may directly contribute to atherosclerotic cardiovascular disease (CVD). Lipotoxic free fatty acid delivery to nonadipose body organs (e.g. liver, muscle, and pancreas) may indirectly contribute to CVD by promoting the most common metabolic disorders encountered in clinical practice (e.g. high blood sugars, high blood pressure, and dyslipidaemia), all major CVD risk factors. Finally, SAT energy overflow may increase VAT accumulation, which is also associated with increased risk of metabolic diseases and CVD. SUMMARY Increased VAT is a surrogate marker for SAT dysfunction which increases waist circumference, reflecting a shared pathologic process leading to the pathogenic fat accumulation of other fat depots and fatty infiltration of nonadipose body organs. Central obesity is a clinical marker for adiposopathy.