JCEM: 高强度运动减少肌肉中IP6K1含量还提高胰岛素抵抗?

2018-01-02 MedSci MedSci原创

众所周知骨骼肌中的胰岛素抵抗可以导致全身的高血糖和与2型糖尿病相关的继发性并发症。肌醇六磷酸激酶-1(IP6K1)可以抑制这种组织中的胰岛素刺激的葡萄糖转运。近日在JCEM上发表的一篇文章则旨在研究肌肉与血浆IP6K1与胰岛素抵抗的高胰岛素血症个体的葡萄糖控制的二室模型是否相关;并对肌肉IP6K1也进行了两个不同的运动试验。

众所周知骨骼肌中的胰岛素抵抗可以导致全身的高血糖和与2型糖尿病相关的继发性并发症。肌醇六磷酸激酶-1(IP6K1)可以抑制这种组织中的胰岛素刺激的葡萄糖转运。近日在JCEM上发表的一篇文章则旨在研究肌肉与血浆IP6K1与胰岛素抵抗的高胰岛素血症个体的葡萄糖控制的二室模型是否相关;并对肌肉IP6K1也进行了两个不同的运动试验。

研究人员纳入了9个糖尿病前期(HbA1c; 6.1(0.2)%)的志愿者进行了一项休息控制、连续运动(乳酸阈值的90%)和高强度的运动试验(6 x 30秒冲刺)。在每个60分钟的试验之前和之后绘制肌肉活检标本图。在第二个肌肉样本后立即进行标记的([6,62H2]葡萄糖)静脉葡萄糖耐量试验(IVGTT)。

研究结果显示空腹肌肉IP6K1含量与胰岛素敏感性SI2 *无相关性(P = 0.961)。高强度运动减少IP6K1肌肉蛋白和mRNA表达(P = 0.001)。连续运动后对蛋白质IP6K1含量没有影响。高强度运动后Akt308的磷酸化明显增加。在同样的试验之后,间歇运动减少肝葡萄糖生产(HGP)。相同的干预措施也改善了SI2 *,且与连续运动改善相比显着更大。我们的体外实验证明,IP6K1的化学抑制增加了C2C12肌管中的胰岛素信号传导。

从上述研究可以看出使用的体内和体外方法表明肌肉IP6K1的减少可能与SI2 *的全身改善相关。此外,高强度运动可降低胰岛素抵抗者的HPG。

原始出处:

Jane Naufahu.et al. High intensity exercise decreases IP6K1 muscle content & improves insulin sensitivity (SI2?)in glucose intolerant individuals. J Clin Endocrinol Metab. 2017.

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    2018-04-06 smallant2015
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    2018-06-06 baoya
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    2018-05-02 achengzhao
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    2018-01-11 wzb521zf

    一起学习学习

    0

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    2018-01-04 aids219

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