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首页> 外文期刊>Cellular Physiology and Biochemistry >Advanced oxidation protein products induce inflammatory response and insulin resistance in cultured adipocytes via induction of endoplasmic reticulum stress
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Advanced oxidation protein products induce inflammatory response and insulin resistance in cultured adipocytes via induction of endoplasmic reticulum stress

机译：先进的氧化蛋白产物通过诱导内质网应激来诱导培养的脂肪细胞中的炎症反应和胰岛素抵抗

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摘要

Accumulation of advanced oxidation protein products (AOPPs) is prevalent in metabolic syndrome and type 2 diabetes. Adipocyte dysfunction has been recognized as a link between these conditions. To examine the effect of AOPPs on adipocyte perturbation, 3T3-L1 adipocytes were treated with increased levels of AOPPs as seen in these conditions. Exposure of adipocytes to AOPPs induced overexpression of tumor necrosis factor α and interleukin-6. This inflammatory response was completely blocked by nuclear factor-κB inhibitor SN50. AOPPs challenge also impaired insulin signaling, which was partly prevented by SN50. Treatment with AOPPs triggered endoplasmic reticulum (ER) stress, revealed by phosphorylation of PKR-like eukaryotic initiation factor 2α kinase, eukaryotic translational initiation factor 2α, inositol-requiring enzyme 1 and c-jun N-terminal kinase, and by overexpression of glucose regulated protein 78. AOPPs-induced ER stress was mediated by reactive oxygen species (ROS) generated by activation of NADPH oxidase since it was prevented by NADPH oxidase inhibitors or ROS scavenger. Treating the cells with inhibitors of NADPH oxidase or ER stress could completely abolish AOPPs-induced overexpression of adipocytokines and insulin resistance, suggesting that AOPPs induced adipocyte perturbation probably through induction of ROS-dependent ER stress. Our data identified AOPPs as a class of important mediator of adipocyte perturbation. Accumulation of AOPPs might be involved in adipocyte dysfunction as seen in metabolic syndrome and type 2 diabetes.
机译：在代谢综合征和2型糖尿病中，高级氧化蛋白产物（AOPP）的积累非常普遍。脂肪细胞功能障碍已被认为是这些状况之间的联系。为了检查AOPP对脂肪细胞摄动的影响，在这些情况下，将3T3-L1脂肪细胞用增加水平的AOPP处理。脂肪细胞暴露于AOPPs会导致肿瘤坏死因子α和白介素6的过度表达。这种炎症反应被核因子-κB抑制剂SN50完全阻断。 AOPPs的挑战也损害了胰岛素信号传导，这部分被SN50阻止。 AOPP的处理触发了内质网（ER）应激，通过PKR样真核生物起始因子2α激酶，真核翻译起始因子2α，需要肌醇的酶1和c-jun N端激酶的磷酸化以及葡萄糖过表达来揭示蛋白质78. AOPP诱导的内质网应激是由NADPH氧化酶活化产生的活性氧（ROS）介导的，因为它可以被NADPH氧化酶抑制剂或ROS清除剂阻止。用NADPH氧化酶或ER应激抑制剂处理细胞可以完全消除AOPPs引起的脂肪细胞因子和胰岛素抵抗的过度表达，这表明AOPPs可能通过诱导ROS依赖性ER应激来诱导脂肪细胞摄动。我们的数据确定了AOPPs是脂肪细胞摄动的重要介体。如代谢综合征和2型糖尿病中所见，AOPP的积累可能与脂肪细胞功能障碍有关。

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