The role of adipose tissue in endothelial dysfunction, etherosclerosis and other complications of metabolic syndrome: influence of diet and pharmacotherapy

The metabolic effects of obesity have made this disease one of the most common risk factors for diabetes, hypertension, and atherosclerosis. Adipose tissue is now recognized as an active secretory and immune organ. Chronic inflammation is a common feature of the obesity, and inflammatory signals may originate within visceral adipose tissue as this fat depot expands in response to chronic positive energy balance. Both adipocytes and macrophages within fat secrete numerous hormones and cytokines that have local effects on WAT physiology but also systemic effects on other organs and may markedly contribute to the development of pathophysiological disorders associated with metabolic syndrome. On the contrary, leanness as well as significant weight reduction in obese patients increases production and circulating levels of metabolically beneficial factors and decreases production of proinflammatory and insulin resistance-inducing factors. Endothelial dysfunction and inflammation are important signs of vascular risk and worsened prognosis in patients with metabolic syndrome and type 2 diabetes. Measures of endothelial function remain invaluable for research into disease mechanism and response to new therapies. An interesting area of ongoing investigation is the role of thiazolidinediones in improving endothelial..