Metabolic syndrome (MS) or insulin resistance syndrome is the result of multiple metabolic abnormalities associated with cardiovascular disease. Since 1988, when Reaven first described MS, many researches have been conducted in order to understand its pathophysiology, epidemiology, prognostic implications and therapeutic strategies. Numerous metabolic abnormalities found in the metabolic syndrome, including hyperglycemia, excessive fatty acids and insulin resistance, cause an endothelial cell dysfunction by affecting nitric oxide synthesis or degradation. Although the exact mechanism by which metabolic syndrome induces endothelial dysfunction remains to be clarified, there are many possibilities of vascular endothelial damage and increase in cardiovascular risk in these patients. The most frequent metabolic, hormonal, hemostatic abnormalities in patients with metabolic syndrome that may contribute to endothelial dysfunction are: hyperinsulinemia, hyperglycemia, increase in fatty acid levels, hypertriglyceridemia, decrease in HDL-cholesterol, increase in small dense LDL-cholesterol, increase in apolipoprotein B, increase in insulin-1 growth factor levels, increase in tissue angiotensin II levels, increase in plasminogen activator inhibitor-1, increase in C reactive protein, increase in oxidative stress.