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Metabolic syndrome and endothelial dysfunction Volume 17, issue 2, Février 2005

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Authors
Service de diabétologie-nutrition, Service des explorations fonctionnelles vasculaires, Service de pharmacologie, CHU Hôtel-Dieu, 49033 Angers Cedex 01

The metabolic syndrome, which interlinks abdominal obesity, insulin resistance with or without the presence of hyperglycaemia, dyslipidaemia and hypertension, is observed in more than one quarter of all adults over the age of 40 years. Its presence encourages cardiovascular disease and type 2 diabetes. Endothelial dysfunction, occurring primarily as a result of a reduction in nitric oxide (NO) bioavailability, represents the earliest abnormality involved in the vascular attack. The functional examination of endothelial-dependant vasomotricity enables early detection of subjects in whom general vascular risk is increased. All components of the metabolic syndrome cause an alteration of endothelial function. The accumulation of visceral adipose tissue, responsible for the development of the metabolic syndrome, also adversely affects endothelial function. Abdominal obesity is associated with a decrease in plasma adiponectin concentration, an adipocyte-secreted protein that induces a favourable effect on vascular walls. Therapy care involves the use of drugs that have been shown to reduce vascular risk, some of which beneficially affect endothelial function. Such treatment shows its true benefit only when integrated as part of general diet and lifestyle care in which the objective is to decrease abdominal fat, thereby acting at the very source of the metabolic syndrome and vascular risk.