通过GPR81激活在肝细胞中乳酸诱导的脂质积累
Giang Nguyen1, Ji Hee Yu2, Phuc Thi Minh Pham1
1Department of Internal Medicine, Kangwon National University School of Medicine, Chuncheon, Korea.
Diabetes & metabolism journal
|November 27, 2025
概括
乳酸盐通过GPR81-AMPK通路促进肝脏脂肪的积累,独立于MCT1运输. 这突出了GPR81作为非酒精性脂肪肝疾病 (NAFLD) 的潜在治疗点.
科学领域:
- 代谢调节 代谢调节 代谢调节
- 肝病学 肝病学是一种肝病学.
- 分子信号传输的方法
背景情况:
- 乳酸盐被认为是代谢调节中的信号分子.
- 乳酸通过G蛋白结合受体81 (GPR81) 在肝肥胖症中的作用尚不清楚.
研究的目的:
- 为了研究乳酸盐对肝脂代谢的影响.
- 阐明GPR81和5'腺单酸活性蛋白激酶 (AMPK) 在乳酸诱导的肝硬化症中信号传导的作用.
主要方法:
- 使用AML12细胞,斑马鱼和饮食诱导的非酒精性脂肪性肝病 (NAFLD) 鼠标模型的体外研究.
- 对脂质积累,基因/蛋白质表达和AMPK信号的评估.
- 实验性操纵包括乳酸暴露,GPR81敲击,MCT1抑制和AMPK激活.
主要成果:
- 乳酸酸增加了de novo脂质生成和脂肪酸吸收,同时降低了脂肪酸氧化和肝细胞中的AMPK酸化,由GPR81.1介导.
- AMPK激活减少了乳酸诱导的脂质积累.
- 乳酸治疗增加了斑马鱼的肝脂含量,在NAFLD小鼠模型中增加了肝乳酸和GPR81.
结论:
- 乳酸盐通过GPR81-AMPK信号轴促进肝硬化.
- 激活GPR81可以独立于MCT1.1,增强脂质生成和脂质吸收.
- GPR81代表了NAFLD的潜在治疗目标.
关键词:
由AMP激活的蛋白质激酶被AMP激活人类HCAR1蛋白质,人类牛奶酸是什么 牛奶酸是什么脂质生殖 (Lipogenesis) 是一种非酒精性脂肪肝疾病是非酒精性脂肪肝疾病.斑马鱼是一种斑马鱼.更多相关视频
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