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首页> 外文期刊>Molecular and Cellular Biology >Separation of Insulin Signaling into Distinct GLUT4 Translocation and Activation Steps
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Separation of Insulin Signaling into Distinct GLUT4 Translocation and Activation Steps

机译：将胰岛素信号分离为不同的GLUT4易位和激活步骤

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GLUT4 (glucose transporter 4) plays a pivotal role in insulin-induced glucose uptake to maintain normal blood glucose levels. Here, we report that a cell-permeable phosphoinositide-binding peptide induced GLUT4 translocation to the plasma membrane without inhibiting IRAP (insulin-responsive aminopeptidase) endocytosis. However, unlike insulin treatment, the peptide treatment did not increase glucose uptake in 3T3-L1 adipocytes, indicating that GLUT4 translocation and activation are separate events. GLUT4 activation can occur at the plasma membrane, since insulin was able to increase glucose uptake with a shorter time lag when inactive GLUT4 was first translocated to the plasma membrane by pretreating the cells with this peptide. Inhibition of phosphatidylinositol (PI) 3-kinase activity failed to inhibit GLUT4 translocation by the peptide but did inhibit glucose uptake when insulin was added following peptide treatment. Insulin, but not the peptide, stimulated GLUT1 translocation. Surprisingly, the peptide pretreatment inhibited insulin-induced GLUT1 translocation, suggesting that the peptide treatment has both a stimulatory effect on GLUT4 translocation and an inhibitory effect on insulin-induced GLUT1 translocation. These results suggest that GLUT4 requires translocation to the plasma membrane, as well as activation at the plasma membrane, to initiate glucose uptake, and both of these steps normally require PI 3-kinase activation.
机译：GLUT4（葡萄糖转运蛋白4）在胰岛素诱导的葡萄糖摄取中发挥关键作用，以维持正常的血糖水平。在这里，我们报告细胞渗透性磷酸肌醇结合肽诱导GLUT4易位至质膜，而不会抑制IRAP（胰岛素反应性氨基肽酶）的内吞作用。但是，与胰岛素治疗不同，肽治疗不会增加3T3-L1脂肪细胞中的葡萄糖摄取，表明GLUT4易位和激活是独立的事件。 GLUT4激活可发生在质膜上，因为当非活性GLUT4首先通过用这种肽预处理细胞而将其转移到质膜时，胰岛素能够以较短的时间延迟增加葡萄糖的摄取。抑制磷脂酰肌醇（PI）3-激酶的活性不能抑制该肽对GLUT4的转运，但是当在肽处理后添加胰岛素时，确实抑制了葡萄糖的摄取。胰岛素而不是肽刺激GLUT1易位。令人惊讶地，肽预处理抑制了胰岛素诱导的GLUT1易位，表明该肽处理对GLUT4易位既具有刺激作用又对胰岛素诱导的GLUT1易位具有抑制作用。这些结果表明，GLUT4需要转运到质膜上，以及在质膜上活化才能启动葡萄糖摄取，并且这两个步骤通常都需要PI 3-激酶活化。

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