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首页> 外文期刊>Molecular and Cellular Biology >ADP-Ribosylation Factor 6 Delineates Separate Pathways Used by Endothelin 1 and Insulin for Stimulating Glucose Uptake in 3T3-L1 Adipocytes
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ADP-Ribosylation Factor 6 Delineates Separate Pathways Used by Endothelin 1 and Insulin for Stimulating Glucose Uptake in 3T3-L1 Adipocytes

机译：ADP核糖基化因子6描绘了内皮素1和胰岛素用于刺激3T3-L1脂肪细胞摄取葡萄糖的单独途径

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In 3T3-L1 adipocytes, both insulin and endothelin 1 stimulate glucose transport via translocation of the GLUT4 glucose carrier from an intracellular compartment to the cell surface. Yet it remains uncertain as to whether both hormones utilize identical pathways and to what extent each depends on the heterotrimeric G protein Gαq as an intermediary signaling molecule. In this study, we used a novel inducible system to rapidly and synchronously activate expression of a dominant inhibitory form of ADP-ribosylation factor 6, ARF6(T27N), in 3T3-L1 adipocytes and assessed its effects on insulin- and endothelin-stimulated hexose uptake. Expression of ARF6(T27N) in 3T3-L1 adipocytes was without effect on the ability of insulin to stimulate either 2-deoxyglucose uptake or the translocation of GLUT4 or GLUT1 to the plasma membrane. However, the same ARF6 inhibitory mutant blocked the stimulation of hexose uptake and GLUT4 translocation in response to either endothelin 1 or an activated form of Gαq, Gαq(Q209L). These results suggest that endothelin stimulates glucose transport through a pathway that is distinct from that utilized by insulin but is likely to depend on both a heterotrimeric G protein from the Gq family and the small G protein ARF6. These data are consistent with the interpretation that endothelin and insulin stimulate functionally different pools of glucose transporters to be redistributed to the plasma membrane.
机译：在3T3-L1脂肪细胞中，胰岛素和内皮素1都通过GLUT4葡萄糖载体从细胞内区室到细胞表面的转运来刺激葡萄糖转运。然而，关于两种激素是否利用相同的途径以及每种激素在多大程度上取决于异源三聚体G蛋白Gαq作为中间信号分子，仍不确定。在这项研究中，我们使用了一种新型的诱导系统来快速同步激活3T3-L1脂肪细胞中ADP-核糖基化因子6，ARF6（T27N）的主要抑制形式的表达，并评估了其对胰岛素和内皮素刺激的己糖的影响摄取。 ARF6（T27N）在3T3-L1脂肪细胞中的表达对胰岛素刺激2-脱氧葡萄糖摄取或GLUT4或GLUT1向质膜移位的能力没有影响。然而，相同的ARF6抑制突变体响应内皮素1或激活形式的Gαq，Gαq（Q209L）阻止了己糖摄取和GLUT4易位的刺激。这些结果表明，内皮素通过不同于胰岛素所利用的途径刺激葡萄糖转运，但是可能既依赖于来自Gq家族的异源三聚体G蛋白又依赖于小G蛋白ARF6。这些数据与内皮素和胰岛素刺激功能不同的葡萄糖转运蛋白池重新分配到质膜的解释一致。

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