Intra-abdominal adiposity, abdominal obesity, and cardiometabolic risk

Preferential fat deposition in the abdomen-between and within viscera-has been linked with cardiometabotic risk. We review data obtained in vivo in subjects with obesity and/or diabetes using magnetic resonance imaging (to quantify fat depots), and positron emitting tomography to quantify glucose uptake ((18)FDG) and blood flow ((H2O)-O-15) under conditions of euglycaemic hyperinsulinaemia (clamp technique). Abdominal visceral adipose tissue (VAT) is small in amount, is dependent on sex, body mass index, and age and is variably related to waist circumference. VAT is inherently more insulin-sensitive than subcutaneous fat; both show impaired glucose uptake in conditions of whole-body insulin resistance. Furthermore, in VAT, insulin sensitivity declines with mass and is directly related to blood flow, possibly reflecting the cellular phenotype of hypertrophic adipose tissue. Nevertheless, in obesity the expanded fat mass makes a greater contribution to overall glucose disposal, thereby providing a compensatory mechanism to the insulin resistance of glucose metabolism. Fat accumulation impairs the ability of target tissues to respond to insulin. On the other hand, it provides a safe repository for excess calories and glucose. The balance between the two sides may set individual disease risk. Fat deposition in 'forbidden' sites (VAT, liver) signals risk well beyond the amount of fat itself.