电脉冲刺激以 Rac-Akt 依赖的方式诱导 C2C12 肌管中的 GLUT4 易位。
Electrical pulse stimulation induces GLUT4 translocation in a Rac-Akt-dependent manner in C2C12 myotubes.
机构信息
Department of Immunology, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital, Tianjin Medical University, China.
Cell Biology Program, The Hospital for Sick Children, Toronto, ON, Canada.
出版信息
FEBS Lett. 2018 Feb;592(4):644-654. doi: 10.1002/1873-3468.12982. Epub 2018 Feb 15.
Muscle contraction increases skeletal muscle glucose uptake, but the underlying mechanisms are not fully elucidated. While important for insulin-stimulated glucose uptake, the role of Akt in contraction-stimulated muscle glucose uptake is controversial. In our study, C2C12 skeletal muscle myotubes were contracted by electrical pulse stimulation (EPS). We found that EPS leads to Akt phosphorylation on sites S473 and T308 in a time-dependent manner. The Akt inhibitor MK2206 partly reduces EPS-stimulated GLUT4 translocation without affecting EPS-stimulated AMPK phosphorylation. EPS activates Rac1 GTP-binding, and EPS-stimulated GLUT4 translocation is partly inhibited by Rac1 inhibitor II and siRac1. Interestingly, both Rac1 inhibitor II and siRac1 inhibit EPS-stimulated Akt phosphorylation on sites S473 and T308. Our findings implicate a Rac1-Akt signaling pathway in EPS-stimulated GLUT4 translocation in C2C12 myotubes.
肌肉收缩增加骨骼肌葡萄糖摄取，但其中的机制尚未完全阐明。虽然 Akt 在胰岛素刺激的葡萄糖摄取中很重要，但它在收缩刺激肌肉葡萄糖摄取中的作用存在争议。在我们的研究中，使用电脉冲刺激（EPS）使 C2C12 骨骼肌肌管收缩。我们发现，EPS 以时间依赖性方式导致 Akt 在 S473 和 T308 位点上的磷酸化。Akt 抑制剂 MK2206 部分减少了 EPS 刺激的 GLUT4 易位，而不影响 EPS 刺激的 AMPK 磷酸化。EPS 激活 Rac1 GTP 结合，Rac1 抑制剂 II 和 siRac1 部分抑制了 EPS 刺激的 GLUT4 易位。有趣的是，Rac1 抑制剂 II 和 siRac1 均抑制了 EPS 刺激的 Akt 在 S473 和 T308 位点上的磷酸化。我们的研究结果表明，Rac1-Akt 信号通路参与了 C2C12 肌管中 EPS 刺激的 GLUT4 易位。
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