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Cdo1-Camkk2-AMPK轴赋予运动在小鼠中对NAFLD的保护作用

Min Chen^1,2,3, Jie-Ying Zhu^1,2,3, Wang-Jing Mu^1,2,3

¹School of Exercise and Health and Collaborative Innovation Center for Sports and Public Health, Shanghai University of Sport, Shanghai, 200438, China.

Nature communications

|December 18, 2023

概括

运动通过增强1型 (Cdo1) 肝系氨基酸二氧化酶的活性来对抗非酒精性脂肪性肝病 (NAFLD). Cdo1增强新陈代谢和脂肪氧化,这对于运动至关重要.

科学领域:

分子生物学分子生物学
代谢性疾病研究研究
运动生理学运动生理学

背景情况:

非酒精性脂肪肝 (NAFLD) 是一个日益严重的健康问题.
运动是已知的NAFLD的非药物治疗方法.
运动与NAFLD改善的确切分子机制尚未完全理解.

研究的目的:

研究氨酸二氧化酶1型 (Cdo1) 在NAFLD中的作用.
阐明运动改善NAFLD的机制.
探索Cdo1作为NAFLD的潜在治疗点.

主要方法:

通过cAMP/PKA/CREB通路检查了运动诱导的肝脏Cdo1表达.
使用肝细胞特异性Cdo1淘汰 (Cdo1^LKO) 和过度表达 (Cdo1^LTG) 的小鼠模型.
研究了Cdo1与Camkk2和AMPK信号的相互作用.

主要成果:

运动通过cAMP/PKA/CREB通路提高肝脏Cdo1的调节.
缺乏Cdo1会影响对NAFLD的运动效益,并降低新陈代谢率.
过度表达Cdo1可以提高代谢率,并与运动协同治疗NAFLD.
Cdo1通过将Camkk2连接到AMPK来激活AMPK信号,促进脂肪酸氧化和线粒体生物发生.

结论:

Cdo1是运动对NAFLD有益影响的关键下游媒介.
Cdo1促进肝脏Camkk2-AMPK信号传递,增强脂肪酸氧化和线粒体功能.
准Cdo1可能为管理NAFLD提供一种新的治疗策略.

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