氧化应激
内分泌学
脂联素
内科学
脂肪因子
脂肪组织
代谢综合征
NADPH氧化酶
脂肪变性
瘦素
化学
生物
胰岛素抵抗
医学
胰岛素
肥胖
作者
Shigetada Furukawa,Takuya Fujita,Michio Shimabukuro,Masanori Iwaki,Yukio Yamada,Yutaka Nakajima,Osamu Numata,Makoto Makishima,Morihiro Matsuda,Iichiro Shimomura
摘要
Obesity is a principal causative factor in the development of metabolic syndrome. Here we report that increased oxidative stress in accumulated fat is an important pathogenic mechanism of obesity-associated metabolic syndrome. Fat accumulation correlated with systemic oxidative stress in humans and mice. Production of ROS increased selectively in adipose tissue of obese mice, accompanied by augmented expression of NADPH oxidase and decreased expression of antioxidative enzymes. In cultured adipocytes, elevated levels of fatty acids increased oxidative stress via NADPH oxidase activation, and oxidative stress caused dysregulated production of adipocytokines (fat-derived hormones), including adiponectin, plasminogen activator inhibitor-1, IL-6, and monocyte chemotactic protein-1. Finally, in obese mice, treatment with NADPH oxidase inhibitor reduced ROS production in adipose tissue, attenuated the dysregulation of adipocytokines, and improved diabetes, hyperlipidemia, and hepatic steatosis. Collectively, our results suggest that increased oxidative stress in accumulated fat is an early instigator of metabolic syndrome and that the redox state in adipose tissue is a potentially useful therapeutic target for obesity-associated metabolic syndrome.
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