The metabolic syndrome is a cluster of risk factors for coronary heart disease that seemingly have an underlying metabolic causation. Central obesity is the centerpiece of the metabolic alterations. Accordingly, increased abdominal adiposity contributes to dyslipidemia, hyperglycemia, and hypertension. In about 20% of the cases with metabolic syndrome, there is also beta-cell dysfunction that leads to the clinical manifestation of diabetes mellitus. Recent evidence suggests that increased obesity is also associated with inflammation. The role of adipose tissue in the causation of metabolic alterations that lead to the clinical manifestation of the metabolic syndrome has become a focus of active research. Adipose tissue not only secretes non-esterified fatty acids that contribute to atherogenic dyslipidemia, steatosis and lipotoxicity. This organ is also an active endocrine and paracrine system. It can secrete pro-inflammatory factors, pro-insulin resistance factors, and other cytokines and hormones that can contribute to hypertension and impaired fibrinolysis. Therefore, the metabolic alterations commonly associated with increased central obesity of the metabolic syndrome are pro-atherogenic partly because the metabolites are proinflammatory.