Abstract
The metabolic syndrome (MetS) represents a combination of cardiovascular risk determinants such as obesity, insulin resistance and lipid abnormalities such as hypertriglyceridemia, increased free fatty acids, low high-density-cholesterol and hypertension. As a multiple component condition it imparts a doubling of relative risk for atherosclerotic cardiovascular disease (ASCVD). It is currently controversial which component of the syndrome carries what weight. There is even a considerable debate whether the risk for ASCVD is greater in patients diagnosed with MetS than that by the individual risk factors. At present, no unifying pathogenetic mechanism can explain the metabolic syndrome and there is no unique treatment for it. This review summarizes and critically reviews the currently available clinical and scientific evidence for the concept that the MetS is causally an endocrine disease and discusses pharmacotherapeutic strategies targeting the pathogenesis rather than single symptoms of the cluster.
