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Obesity and endothelial dysfunction

Obesity is an independent risk factor for cardiovascular disease (CVD), although mechanisms linking obesity and risk for CVD are not completely understood. Recent studies have indicated that accumulation of adipose tissue is characterized by chronic low-grade inflammation. In obesity adipose tissue becomes dysfuntional, resulting in an overproduction of proimmflamatory adipokines and a lower production of ant- inflammatory adipokines. There is a large body of evidence that endothelial dysfunction precedes and predicts clinical disease, suggesting that endothelial dysfunction and impaired vascular reactivity is an initial step in development of cardiovascular complications caused by obesity. A growing body of evidence implicates adipose tissue in general, and visceral adiposity in particular, as key regulators of inflammation. Our study results demonstrated that endothelium-dependent, flow- and acetylcholine- induced, dilation are reduced in resistance arteries from visceral compared to subcutaneous adipose tissue in morbidly obese woman, which is consistent with previous demonstrations of endothelial dysfunction in obesity. An increase in oxidative stress appears to be a major mechanism underlying the development of vascular endothelial dysfunction. The dominant mechanism responsible for endothelial dysfunction is the decrease in bioavailable of nitric oxide (NO), as well as the increase in reactive oxygen species (ROS) production and apoptosis. This increases contractility, and with increased inflammation may predispose to cardiovascular disease such as hypertension. Recent epidemiologic data indicate that the prevalence of hypertension in severely obese persons is more than 60%. A unique subset of obese individuals display a favourable metabolic profile, characterised by high levels of insulin sensitivity, normal lipid and inflammation profiles and no sign of hypertension, despite having excessive body fatness, they are metabollicaly healthy obese (MHO) individuals. Studies have shown that MHO humans are at lower risk than than at risk obese individuals, but at higher risk than the general population. Studies that examined vascular endothelial function demonstrated that flow-mediated dilation was significantly lower in MHO then in lean individuals, despite a normal metabolic profile and normotensity. Although the importance of obesity as a major cause of essential hypertension is well established, the physiological and molecular mechanisms involved in that occurence are only beginning to be elucidated.

obesity; endothelial dysfunction; oxidative stress

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