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首页> 外文期刊>Pathobiology: journal of immunopathology, molecular and cellular biology >Uniaxial cyclic stretch-stimulated glucose transport is mediated by a ca-dependent mechanism in cultured skeletal muscle cells.
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Uniaxial cyclic stretch-stimulated glucose transport is mediated by a ca-dependent mechanism in cultured skeletal muscle cells.

机译：在培养的骨骼肌细胞中，单轴循环拉伸刺激的葡萄糖转运是由ca依赖性机制介导的。

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OBJECTIVE: Mechanical stimuli such as stretch increase glucose transport and glycogen metabolism in skeletal muscle. However, the molecular mechanisms involved in the mechanotransduction events are poorly understood. The present study was conducted in order to determine whether the signaling mechanism leading to mechanical stretch-stimulated glucose transport is similar to, or distinct from, the signaling mechanisms leading to insulin- and contraction-stimulated glucose transport in cultured muscle cells. METHODS: Cultured C2C12 myotubes were stretched, after which the 2-deoxy-D-glucose (2-DG) uptake was measured. RESULTS: Following cyclic stretch, C2C12 myotubes showed a significant increase in 2-DG uptake, and this effect was not prevented by inhibiting phosphatidylinositol 3-kinase or 5'-AMP-activated protein kinase and by extracellular Ca(2+) chelation. Conversely, the stretch-stimulated 2-DG uptake was completely prevented by dantrolene (an inhibitor of Ca(2+) release from sarcoplasmic reticulum).Furthermore, the stretch-stimulated 2-DG uptake was prevented by the Ca(2+)/calmodulin-dependent kinase inhibitor KN93 which did not prevent the insulin-stimulated 2-DG uptake. CONCLUSIONS: These results suggest that the effects of stretch-stimulated glucose transport are independent of the insulin-signaling pathway. By contrast, following mechanical stretch in skeletal muscle, the signal transduction pathway leading to glucose transport may require the participation of cytosolic Ca(2+) and Ca(2+)/calmodulin kinase, but not 5'-AMP-activated protein kinase.
机译：目的：机械刺激（如拉伸）可增加骨骼肌中的葡萄糖转运和糖原代谢。但是，有关机械转导事件的分子机制了解甚少。进行本研究是为了确定导致机械拉伸刺激的葡萄糖转运的信号传导机制与培养的肌细胞中导致胰岛素和收缩刺激的葡萄糖转运的信号传导机制是否相似或不同。方法：拉伸培养的C2C12肌管，然后测量2-脱氧-D-葡萄糖（2-DG）的摄取。结果：循环拉伸后，C2C12肌管显示2-DG摄取显着增加，并且这种作用不能通过抑制磷脂酰肌醇3激酶或5'-AMP激活的蛋白激酶以及细胞外Ca（2+）螯合来阻止。相反，丹特罗林（一种从肌质网释放Ca（2+）的抑制剂）完全阻止了拉伸刺激的2-DG摄取，此外，Ca（2 +）/阻止了拉伸刺激的2-DG摄取。钙调蛋白依赖性激酶抑制剂KN93，它不能阻止胰岛素刺激的2-DG摄取。结论：这些结果表明，拉伸刺激的葡萄糖转运的作用与胰岛素信号通路无关。相比之下，骨骼肌中的机械拉伸后，导致葡萄糖转运的信号转导途径可能需要胞质Ca（2+）和Ca（2 +）/钙调蛋白激酶的参与，而不是5'-AMP激活的蛋白激酶。

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