HIIT与MICT如何改善T2DM糖代谢?AMPK/PGC-1α信号轴机制解析

2026-03-21 MedSci xAi 发表于广东省
本研究揭示高强度间歇训练(HIIT)和中度持续训练(MICT)通过抑制MSTN表达、激活AMPK/PGC-1α信号轴改善T2DM小鼠糖代谢异常的分子机制。实验数据显示HIIT在提升AMPK磷酸化水平和线粒体质量控制方面显著优于MICT,为糖尿病运动疗法提供新证据。

Compared to the NC group, the protein expression of PGC-1α and AMPK, as well as the phosphorylation level of AMPK, were significantly decreased in the DC group (P<0.001, P<0.01), while the protein expression of MSTN was significantly increased (P<0.01). Compared to the DC group, the protein expression of PGC-1α and the phosphorylation level of AMPK were significantly increased in both the MICT group and the HIIT group (P<0.01, P<0.001), while the protein expression of MSTN was significantly decreased (P<0.001). The protein expression of AMPK did not change significantly in the MICT group but was significantly increased in the HIIT group (P<0.001). Compared to the MICT group, the protein expression of PGC-1α and AMPK, as well as the phosphorylation level of AMPK, were significantly increased in the HIIT group (P<0.01, P<0.05), while the protein expression of MSTN did not change significantly.

Research Conclusions:

  1. High-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) can effectively alleviate glucose metabolism abnormalities in T2DM mice, as evidenced by improvements in body weight, blood glucose levels, and skeletal muscle glucose metabolism function, as well as enhanced mitochondrial quality in skeletal muscle. Additionally, HIIT exhibits superior intervention effects on mitochondrial quality control compared to MICT.
  2. Both high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) improve T2DM skeletal muscle glucose metabolism disorders by inhibiting MSTN expression in skeletal muscle and activating the AMPK/PGC-1α signaling axis, thereby enhancing mitochondrial quality control.
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