Article, see p 48
Obesity is a major risk factor for diabetes mellitus and cardiovascular disease. The societal cost of obesity is keeping pace with the growing scope of the epidemic, estimated to account for ≈17% of all US health expenditures by 2030.1 The clinical burden of obesity-related cardiovascular disease is profound; recent data suggest that severe obesity (body mass index >35 kg/m2) is associated with nearly a 4-fold increased risk of incident heart failure and an ≈2-fold increased risk of incident coronary heart disease and stroke.2 Given the strong associations between obesity and hypertension, diabetes mellitus, and dyslipidemia, it is understandable that much of the obesity-related coronary heart disease risk is attributable to concurrent traditional risk factors such as hypertension, diabetes mellitus, and dyslipidemia. However, data suggest a persistent risk association between obesity and coronary heart disease that is not explained by conventional risk factors, thereby spawning extensive investigations to identify the culprit mechanisms.3 Over the past several decades, the research focus has shifted to the adipose tissues themselves, and more specifically the adipocyte, as a key link between obesity and cardiovascular disease risk.
Adipose tissue functions primarily as a storage depot for excess calories and thus plays an important physiological role to maintain metabolic homeostasis. In healthy (nonobese) states, adipocytes participate in metabolic regulation not only by storing excess calories as lipid, but also by secreting hormones such as leptin that regulate food intake to maintain proper energy balance. When …