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通过抑制ROS/DNA损伤途径,HIGD1A将SIRT1活性与脂肪色联系在一起

Bai-Yu Li¹, Wan-Qiu Peng¹, Yang Liu¹

¹Key Laboratory of Metabolism and Molecular Medicine of the Ministry of Education, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology and Metabolism of Zhongshan Hospital, Fudan University, Shanghai 200032, China.

|July 2, 2023

概括

缺氧诱导的基因域蛋白-1a (HIGD1A) 通过调节线粒体功能来促进脂肪色和热生成. 通过将SIRT1活性与脂肪细胞色联系起来,HIGD1A增强了代谢健康,并预防了饮食引起的肥胖.

科学领域:

代谢健康代谢健康
线粒体生物学线粒体生物学
脂肪组织生物学脂肪组织生物学

背景情况:

分散能量的脂肪细胞 (白色/色细胞) 是改善新陈代谢健康的关键目标.
脂肪棕色化,即将白色转化为棕色类脂肪的过程,增加了能源消耗.
线粒体功能是热生成和代谢调节的核心.

研究的目的:

为了确定脂肪色的新型调节剂.
阐明缺氧诱导的基因域蛋白-1a (HIGD1A) 在脂肪细胞热生成中的作用.
了解将HIGD1A与代谢健康联系起来的分子机制.

主要方法:

在寒冷暴露的反应中研究了HIGD1A表达.
利用基因淘汰和脂肪细胞中的过度表达.
评估了线粒体呼吸,活性氧物种 (ROS) 水平,NAD+/NADH比率和SIRT1活性.
在小鼠中检查了改变HIGD1A水平的发热和饮食诱导的肥胖 (DIO).

主要成果:

HIGD1A是由冷暴露引起的,并积极调节脂肪色.
缺少HIGD1A会损害线粒体呼吸,增加ROS,降低NAD+/NADH比,抑制SIRT1活动和色.
在小鼠中,HIGD1A过度表达促进了色,增强了发热,并防止了DIO.
HIGD1A作为线粒体调节剂,将SIRT1活动与脂肪细胞色联系起来.

结论:

HIGD1A 是脂肪色和热生成的关键积极调节者.
HIGD1A调节线粒体功能以维持代谢平衡.
准HIGD1A可能为肥胖和相关代谢障碍提供治疗策略.

关键词:

CP:新陈代谢过程中的新陈代谢.造成的DNA损伤是DNA损伤.HIGD1A 一个高度.在NAD+) /NADH的比率.这就是ROSOS ROS.一个SIRT1系统.脂肪细胞棕色化脂肪细胞棕色化缺氧诱导的基因域蛋白-1a 在SIRTUIN1中

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