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Prologed Oxidative Stress Impairs Insulin-Induced GLUT4 Translocationin 3T3-L1 Adipocytes

机译:长时间的氧化应激损害胰岛素诱导的GLUT4易位3T3-L1脂肪细胞。

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摘要

Prolonged exposure of 3T3-L1 adipocytes to micromo- lar concentrations of H_2O_2 results in an impaired response to the acutemetabolic effects of insulin. In this study, we further characterized the mechanisms by which oxidative stress impairs insulin stimulation of glucose transport activity. Although insulin induced a 2.5-fold increase in plasma membrane (GLUT4 content and a 50/100 reduction in its abundance in the low-density microsomal (LDM) fraction in control cells, oxidation completely prevented these responses.
机译:3T3-L1脂肪细胞长时间暴露于微摩尔浓度的H_2O_2会导致对胰岛素的急性代谢作用的反应减弱。在这项研究中,我们进一步表征了氧化应激损害胰岛素刺激葡萄糖转运活性的机制。尽管胰岛素在对照细胞的低密度微粒体(LDM)组分中引起质膜(GLUT4含量增加2.5倍,其丰度降低50/100),但氧化完全阻止了这些反应。

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