运动与胰岛素：在 AS160 和 TBC1D1 处趋同还是分歧？
Exercise and insulin: Convergence or divergence at AS160 and TBC1D1?
机构信息
Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, 48109-2214, USA.
出版信息
Exerc Sport Sci Rev. 2009 Oct;37(4):188-95. doi: 10.1097/JES.0b013e3181b7b7c5.
Abstract
Akt substrate of 160 kDa (called AS160 or TBC1D4) and TBC1D1, Rab GTPase-activating proteins that regulate glucose transport, become phosphorylated with exercise or insulin stimulation. Evidence suggests that this convergence may prove to be imperfect, and each stimulus will produce a unique phosphosignature, providing a plausible mechanism for their apparently unique and overlapping roles in exercise- and insulin-stimulated glucose transport.
摘要
Akt 底物 160 kDa（称为 AS160 或 TBC1D4）和 TBC1D1，是调节葡萄糖转运的 Rab GTP 酶激活蛋白，在运动或胰岛素刺激下会发生磷酸化。有证据表明，这种趋同可能并不完美，每个刺激都会产生独特的磷酸化特征，为它们在运动和胰岛素刺激的葡萄糖转运中明显独特且重叠的作用提供了一个合理的机制。
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本文引用的文献
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Am J Physiol Endocrinol Metab. 2009 Jul;297(1):E242-51. doi: 10.1152/ajpendo.00194.2009. Epub 2009 May 12.
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Potential role of TBC1D4 in enhanced post-exercise insulin action in human skeletal muscle.TBC1D4在增强人体骨骼肌运动后胰岛素作用中的潜在作用。
Diabetologia. 2009 May;52(5):891-900. doi: 10.1007/s00125-009-1294-y. Epub 2009 Feb 28.
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Rapid reversal of insulin-stimulated AS160 phosphorylation in rat skeletal muscle after insulin exposure.胰岛素暴露后大鼠骨骼肌中胰岛素刺激的 AS160 磷酸化的快速逆转。
Physiol Res. 2010;59(1):71-78. doi: 10.33549/physiolres.931707. Epub 2009 Feb 27.
4
Inhibition of contraction-stimulated AMP-activated protein kinase inhibits contraction-stimulated increases in PAS-TBC1D1 and glucose transport without altering PAS-AS160 in rat skeletal muscle.收缩刺激的AMP活化蛋白激酶的抑制作用可抑制收缩刺激引起的大鼠骨骼肌中PAS-TBC1D1和葡萄糖转运的增加，而不改变PAS-AS160。
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5
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7
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Am J Physiol Endocrinol Metab. 2008 Jul;295(1):E29-37. doi: 10.1152/ajpendo.90331.2008. Epub 2008 May 13.
10
Discovery of TBC1D1 as an insulin-, AICAR-, and contraction-stimulated signaling nexus in mouse skeletal muscle.TBC1D1作为胰岛素、AICAR和收缩刺激信号枢纽在小鼠骨骼肌中的发现。
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