在维生素D缺乏的小鼠中,运动通过VDR/AMPK介导的自活化减弱了肝脂积累
Jing-Jing Liu1, Yan-Jun Niu1, Xiao-Ning Cui1
1School of Exercise and Health, Shanghai University of Sport, Shanghai, China.
Cellular signalling
|November 25, 2025
概括
运动通过激活VDR/AMPK通路来对抗维生素D缺乏引起的脂肪肝,促进自. 这项研究揭示了炼运动.
科学领域:
- 代谢健康 代谢健康
- 细胞生物学 细胞生物学
- 营养科学 营养科学
背景情况:
- 维生素D缺乏 (VDD) 与脂肪肝疾病有关.
- 运动是一种已知的干预措施,但其在VDD相关肝脏问题中的分子作用尚不清楚.
研究的目的:
- 为了研究运动如何减轻VDD诱导的肝脂积累.
- 阐明涉及维生素D受体 (VDR) 和AMPK介导的自的分子机制.
主要方法:
- 建立了一个VDD小鼠模型,并将它们置于12周的运动中.
- 在AML12细胞中利用lentivirus介导的VDRshRNA来击败VDR.
- 将AMPK激活剂GSK621注射到VDR敲击细胞中.
主要成果:
- 通过增加肝脏VDR和激活AMPK介导的自,运动改善了小鼠的VDD诱导的肝脂积累.
- 在体外,VDR倒置抑制了自和AMPK酸化.
- GSK621治疗逆转了VDR敲击的效果,恢复了自和AMPK酸化.
结论:
- 运动有效地减少了VDD中的脂肪肝积累.
- 该机制涉及维生素D受体 (VDR) 和AMPK介导自的激活.
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