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首页> 美国卫生研究院文献>The Journal of Clinical Investigation >Glucose transport in cultured human skeletal muscle cells. Regulation by insulin and glucose in nondiabetic and non-insulin-dependent diabetes mellitus subjects.
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Glucose transport in cultured human skeletal muscle cells. Regulation by insulin and glucose in nondiabetic and non-insulin-dependent diabetes mellitus subjects.

机译：培养的人骨骼肌细胞中的葡萄糖转运。非糖尿病和非胰岛素依赖型糖尿病患者的胰岛素和葡萄糖调节。

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A primary human skeletal muscle culture (HSMC) system, which retains cellular integrity and insulin responsiveness for glucose transport was employed to evaluate glucose transport regulation. As previously reported, cells cultured from non-insulin-dependent diabetic (NIDDM) subjects displayed significant reductions in both basal and acute insulin-stimulated transport compared to nondiabetic controls (NC). Fusion/differentiation of NC and NIDDM HSMC in elevated media insulin (from 22 pM to 30 microM) resulted in increased basal transport activities but reduced insulin-stimulated transport, so that cells were no longer insulin responsive. After fusion under hyperinsulinemic conditions, GLUT1 protein expression was elevated in both groups while GLUT4 protein level was unaltered. Fusion of HSMC under hyperglycemic conditions (10 and 20 mM) decreased glucose transport in NC cells only when combined with hyperinsulinemia. Hyperglycemia alone down-regulated transport in HSMC of NIDDM, while the combination of hyperglycemia and hyperinsulinemia had greater effects. In summary: (a) insulin resistance of glucose transport can be induced in HSMC of both NC and NIDDM by hyperinsulinemia and is accompanied by unaltered GLUT4 but increased GLUT1 levels; and (b) HSMC from NIDDM subjects demonstrate an increased sensitivity to impairment of glucose transport by hyperglycemia. These results indicate that insulin resistance in skeletal muscle can be acquired in NC and NIDDM from hyperinsulinemia alone but that NIDDM is uniquely sensitive to the additional influence of hyperglycemia.
机译：保留细胞完整性和胰岛素对葡萄糖转运的反应性的主要人类骨骼肌培养（HSMC）系统用于评估葡萄糖转运调节。如先前报道，与非糖尿病对照（NC）相比，从非胰岛素依赖型糖尿病（NIDDM）受试者培养的细胞显示基础和急性胰岛素刺激的转运均显着降低。 NC和NIDDM HSMC在升高的培养基胰岛素（从22 pM到30 microM）中的融合/分化导致基础转运活性增加，但胰岛素刺激的转运减少，因此细胞不再对胰岛素有反应。在高胰岛素条件下融合后，两组的GLUT1蛋白表达均升高，而GLUT4蛋白水平未改变。只有在合并高胰岛素血症的情况下，在高血糖条件下（10和20 mM）的HSMC融合才能降低NC细胞中的葡萄糖转运。单独的高血糖会下调NIDDM在HSMC中的转运，而高血糖和高胰岛素血症的结合则具有更大的作用。总结：（a）高胰岛素血症可在NC和NIDDM的HSMC中诱导葡萄糖转运的胰岛素抵抗，并伴有GLUT4不变但GLUT1水平升高； （b）来自NIDDM受试者的HSMC显示出对高血糖损害葡萄糖转运的敏感性增加。这些结果表明，仅通过高胰岛素血症就可以在NC和NIDDM中获得骨骼肌的胰岛素抵抗，但NIDDM对高血糖的其他影响具有独特的敏感性。

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