How Would Metabolic Syndrome Disturb the Normal Endothelial Function?

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Metabolic syndrome (MetS) is an escalating epidemic that could influence more than one billion people worldwide. It is expressed as the presence of visceral obesity, hyperglycemia, dyslipidemia, and elevated blood pressure. MetS is a multifactorial disorder affecting all features of the community and extensively affects morbidity and mortality. Independently, the constituents of metabolic syndrome have the potential to influence the endothelium causing vascular dysfunction and interrupt vascular homeostasis. Since all components of MetS have unfavorable effects on the endothelium, endothelial dysfunction is more prevalent in MetS patients. Endothelial dysfunction could be a part of the pathogenesis of atherosclerosis in MetS. The nominated mechanisms of endothelial dysfunction linked with MetS are reduced NO production, upraised reactive oxygen species and high production of vasoconstrictors. All the elements of MetS especially the compromised endothelial function could participate in increasing the risks of cardiovascular disease, stroke, myocardial infarction and type 2 DM. Endothelial dysfunction, moreover, stimulates proinflammatory and oxidative stress pathways via endothelial mitochondrial reactive oxygen species (ROS) forcing vascular growth and remodeling. Because MetS is a multifactorial disorder, numerous signaling pathways manipulate the succeeding endothelial dysfunction. In the current review, we will discuss the incidence and pathogenesis of altered endothelial function in MetS. We will also discuss the impending effects of lifestyle measures and pharmacological interventions on endothelial function in patients with MetS .