Glucose transport is rate limiting for dietary glucose utilization by muscle and fat. The glucose transporter GLUT4 is dynamically sorted and retained intracellularly and redistributes to the plasma membrane (PM) by insulin-regulated vesicular traffic, or 'GLUT4 translocation'. Here we emphasize recent findings in GLUT4 translocation research. The application of total internal reflection fluorescence microscopy (TIRFM) has increased our understanding of insulin-regulated events beneath the PM, such as vesicle tethering and membrane fusion. We describe recent findings on Akt-targeted Rab GTPase-activating proteins (GAPs) (TBC1D1, TBC1D4, TBC1D13) and downstream Rab GTPases (Rab8a, Rab10, Rab13, Rab14, and their effectors) along with the input of Rac1 and actin filaments, molecular motors [myosinVa (MyoVa), myosin1c (Myo1c), myosinIIA (MyoIIA)], and membrane fusion regulators (syntaxin4, munc18c, Doc2b). Collectively these findings reveal novel events in insulin-regulated GLUT4 traffic.

中文翻译：

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GLUT4 囊泡流量更新：胰岛素作用的基石

葡萄糖转运限制了肌肉和脂肪对膳食葡萄糖的利用。葡萄糖转运蛋白 GLUT4 在细胞内动态分类和保留，并通过胰岛素调节的囊泡运输或“GLUT4 易位”重新分布到质膜 (PM)。在这里，我们强调 GLUT4 易位研究的最新发现。全内反射荧光显微镜 (TIRFM) 的应用增加了我们对 PM 下胰岛素调节事件的理解，例如囊泡束缚和膜融合。我们描述了 Akt 靶向 Rab GTPase 激活蛋白 (GAP)（TBC1D1、TBC1D4、TBC1D13）和下游 Rab GTPase（Rab8a、Rab10、Rab13、Rab14 及其效应子）以及 Rac1 和肌动蛋白丝的输入的最新发现，分子马达 [myosinVa (MyoVa), myosin1c (Myo1c), myosinIIA (MyoIIA)] 和膜融合调节剂（syntaxin4、munc18c、Doc2b）。总的来说，这些发现揭示了胰岛素调节的 GLUT4 流量中的新事件。