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Reactive oxygen species (ROS) are cellular metabolic products found in the living body. These species play an essential role in physiological system. However, the damage under the oxidative stress possibly occurs if there is imbalance between production of ROS and scavenging capacity. Oxidative stress interferes several biological systems and becomes one important factor in metabolic syndrome such as obesity, diabetes mellitus, and nonalcoholic fatty liver (NAFLD). The linear relationship between increasing body mass index (BMI) and waist circumference and the elevation of lipid peroxidation markers including plasma thiobarbituric acid reactive substances (TBARS) and urine 8-epi-prostaglandin-F2a, with lowering the levels of adiponectin and enzymatic antioxidants, i.e., superoxide dismutase, glutathione peroxidase, and catalase (CAT), has been reported. Correspondingly, levels of TBARS and hydrogen peroxide in plasma and white adipose tissue were increased together with decline of expression of adiponectin and peroxisome proliferator activated receptor gamma (PPAR-g) in the obese and diabetes mice. The expression of tumor necrosis factor alpha (TNF-a), plasminogen activator inhibitor-1 (PAI-1), and nicotinamide adenine dinucleotide phosphate-oxidase (NADPH oxidase) subunits were up-regulated. Furthermore, correlation between elevation of conjugated dienes and malondialdehyde, the index of lipid peroxidation, and attenuation of glutathione and activity of CAT was shown in the patients with NAFLD. Hence, the metabolic syndrome is associated with disequilibrium of anti-oxidation system. The future studies for understanding a variable influencing oxidative stress and pathogenesis of metabolic syndrome are worth interesting for protection and delay progression of metabolic syndrome.
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