The intricate relationship between obesity, diabetes, Metabolic Syndrome, and the consequent development of atherosclerosis has now gained the attention of a substantial part of the scientific community, given their epidemiologic implications. It is accepted that obesity predisposes for the development of diabetes and that these two entities in the same individual will lead to the Metabolic Syndrome. All the clinical characteristic associated with the Metabolic Syndrome have been recognized as major contributors for the development of atherosclerosis and its acute complications. Different definitions of the Metabolic Syndrome exist: one from the 2001 National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP-III), and the other from The World Health Organization (WHO). Regardless of the definition, the net effect of dyslipidemia, hypertension and hyperglycemia results in endothelial cell dysfunction. The consequence of endothelial dysfunction is downregulation of fibrinolysis and upregulation of thrombosis and platelet aggregation. By this mechanism, Metabolic Syndrome unchecked leads to acceleration of atherosclerosis and its subsequent acute complications. Herein, we explore how Metabolic Syndrome, by creating endothelial dysfunction, mechanistically results in alterations in thrombosis and fibrinolysis.
|Original language||English (US)|
|Title of host publication||The Metabolic Syndrome at the Beginning of the XXI Century: A Genetic and Molecular Approach|
|Number of pages||10|
|ISBN (Print)||8481748927, 9788481748925|
|State||Published - Nov 11 2005|
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