ABSTRACT
The prevalence of obesity has escalated dramatically in the United States (1). This has led to a marked increase in the metabolic syndrome, a clustering of atherosclerotic cardiovascular disease (CVD) risk factors characterized by visceral adiposity, hypertension, diabetes, insulin resistance, low high-density lipoprotein (HDL) cholesterol, and a systemic proinflammatory state (2). Although obesity is a powerful risk factor for type 2 diabetes mellitus (DM-2) and CVDs across populations, considerable heterogeneity exists in the relationship between metabolic and cardiovascular abnormalities and the degree of obesity (3). Significant subgroups of subjects who are defined as obese by current guidelines do not develop insulin resistance; conversely, insulin resistance can be present in lean individuals (4). Genetic and environmental factors may have a major impact on the metabolic and cardiovascular consequences of obesity, although the mechanisms by which genetic factors modify the effects of obesity are largely unknown.
