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首页> 外文期刊>Cell metabolism >Rab10, a target of the AS160 Rab GAP, is required for insulin-stimulated translocation of GLUT4 to the adipocyte plasma membrane.
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Rab10, a target of the AS160 Rab GAP, is required for insulin-stimulated translocation of GLUT4 to the adipocyte plasma membrane.

机译：Rab10是AS160 Rab GAP的靶标，是胰岛素刺激的GLUT4转运至脂肪细胞质膜所必需的。

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摘要

GLUT4 trafficking to the plasma membrane of muscle and fat cells is regulated by insulin. An important component of insulin-regulated GLUT4 distribution is the Akt substrate AS160 rab GTPase-activating protein. Here we show that Rab10 functions as a downstream target of AS160 in the insulin-signaling pathway that regulates GLUT4 translocation in adipocytes. Overexpression of a mutant of Rab10 defective for GTP hydrolysis increased GLUT4 on the surface of basal adipocytes. Rab10 knockdown resulted in an attenuation of insulin-induced GLUT4 redistribution to the plasma membrane and a concomitant 2-fold decrease in GLUT4 exocytosis rate. Re-expression of a wild-type Rab10 restored normal GLUT4 translocation. The basal increase in plasma-membrane GLUT4 due to AS160 knockdown was partially blocked by knocking down Rab10 in the same cells, further indicating that Rab10 is a target of AS160 and a positive regulator of GLUT4 trafficking to the cell surface upon insulin stimulation.
机译：GLUT4向肌肉和脂肪细胞质膜的运输受胰岛素调节。胰岛素调节的GLUT4分布的重要组成部分是Akt底物AS160 rab GTPase激活蛋白。在这里，我们显示Rab10在调节脂肪细胞中GLUT4易位的胰岛素信号通路中作为AS160的下游目标。 GTP水解缺陷的Rab10突变体的过表达增加了基础脂肪细胞表面的GLUT4。 Rab10基因敲低导致胰岛素诱导的GLUT4向质膜的重新分布减弱，并伴随GLUT4胞吐速率降低2倍。野生型Rab10的重新表达恢复了正常的GLUT4易位。通过敲低同一细胞中的Rab10，部分阻断了由于AS160敲低引起的血浆膜GLUT4的基础增加，进一步表明Rab10是AS160的靶标，并且是胰岛素刺激后GLUT4转运到细胞表面的阳性调节剂。

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