The metabolic syndrome refers to the clustering of cardiovascular risk factors that include diabetes, obesity, dyslipidaemia and hypertension. Due to various definitions and unexplained pathophysiology it is still a source of medical controversy. Insulin resistance and visceral obesity have been recognized as the most important pathogenic factors. Insulin resistance could be defined as the inability of insulin to produce its numerous actions, in spite of the unimpaired secretion from the beta cells. Metabolic abnormalities result from the interaction between the effects of insulin resistance located primarily in the muscle and adipose tissue and the adverse impact of the compensatory hyperinsulinaemia on tissues that remain normally insulin-sensitive. The clinical heterogeneity of the syndrome can be explained by its significant impact on glucose, fat and protein metabolism, cellular growth and differentiation, and endothelial function. Visceral fat represents a metabolically active organ, strongly related to insulin sensitivity. Moderating the secretion of adipocytokines like leptin, adiponectin, plasminogen activator inhibitor 1 (PAI-1), tumor necrosis factor alfa (TNF-alfa), interleukin-6 (IL-6) and resistin, it is associated with the processes of inflammation, endothelial dysfunction, hypertension and atherogenesis. In 2005, the International Diabetes Federation (IDF) has proposed a new definition, based on clinical criteria and designed for global application in clinical practice. Visceral obesity measured by waist circumference is an essential requirement for diagnosis; other variables include increased triglyceride and decreased HDL levels, hypertension and glucose impairment. Whatever the uncertainties of definition and etiology, metabolic syndrome represents a useful and simple clinical concept which allows earlier detection of type 2 diabetes and cardiovascular disease.