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Measurement of the concentration of C-reactive protein (CRP), (5) an acute-phase reactant, has been used for decades in the diagnosis and monitoring of active infections and chronic inflammatory diseases. Recently, epidemiologic studies have documented that increases in CRP concentrations, even when within the reference interval, can predict the development of type 2 diabetes (1, 2) and cardiovascular disease (CVD) (3) in otherwise healthy adults. Moreover, in addition to being a powerful risk marker, some evidence suggests that CRP directly promotes atherosclerotic processes (4,5). In adults (6-13), plasma CRP concentrations are significantly associated with body fat as well as with specific components of the metabolic syndrome, including systolic blood pressure (BP) and fasting plasma concentrations of insulin, triglycerides (TGs), and HDL-cholesterol (HDL-C). However, the independent contributions of excess adiposity and its frequently associated metabolic abnormalities to variations in CRP values are poorly understood. Some studies suggest that chronic, low-grade inflammation might be an early event in the development of insulin resistance (IR) and the metabolic syndrome (14,15). However, McLaughlin et al. (16) have demonstrated that in healthy obese women, CRP concentrations were increased predominantly among those who were insulin resistant and that the relationship between CRP concentrations and IR was independent of obesity, suggesting that IR and/or other abnormalities associated with the metabolic syndrome might induce inflammatory responses.