通过运动恢复自改善胰岛素抵抗,部分是通过氨酸驱动的TFEB核转移
Ping Wang1, Jiaxin Li1, Chun Guang Li2
1School of Physical Education, Hangzhou Normal University, Hangzhou, China.
Clinical and experimental pharmacology & physiology
|January 9, 2025
概括
运动增强了骨肌肉中的自-溶酶体系统,改善了肥胖小鼠的葡萄糖代谢. 这一过程涉及氨酸介导转录因子EB (TFEB) 的核转位,运动激活了它来对抗胰岛素抵抗.
科学领域:
- 细胞生物学 细胞生物学
- 代谢适应 代谢适应
- 运动生理学 运动生理学
背景情况:
- 众所周知,运动可以激活骨肌肉中的自-溶解体系统,这对代谢适应至关重要.
- 在肥胖引起的胰岛素抵抗的背景下,运动调节这个系统的确切机制尚未完全理解.
研究的目的:
- 研究运动诱导的自和溶酶体系统激活在改善骨肌肉葡萄糖代谢中的作用.
- 阐明分子机制,特别是转录因子EB (TFEB) 和氨酸素在运动介导的代谢改善中的参与.
主要方法:
- 雄性C57BL/6小鼠在12周内接受高脂肪饮食 (HFD),有或没有跑步机炼.
- 特定组接受了FK506,一种氨酸抑制剂,以评估其对炼效果的影响.
- 与自,溶酶体功能和TFEB激活相关的关键蛋白质 (pTFEB,T-TFEB,Beclin1,LC3,ULK1,SQSTM1,LAMP1,CTSD,CTSL) 在胃角肌中进行了分析.
主要成果:
- HFD诱导了胰岛素耐药性和降低了自-溶酶蛋白表达.
- 运动显著增加了TFEB核转位,恢复了自-溶酶蛋白水平,改善了葡萄糖代谢.
- FK506部分抑制了运动诱导的TFEB核转位,表明了氨酸的作用.
结论:
- 运动通过氨酸介导的TFEB核转位促进骨肌肉自和溶酶体恢复.
- 这种机制有助于减轻小鼠的高脂肪饮食引起的胰岛素抵抗.
- 向氨酸-TFEB通路可能为代谢障碍提供治疗策略.
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