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增强的ECCD36信号传递促进了雌性小鼠骨肌肉对胰岛素的抵抗

Austin Dada¹, Javad Habibi^1,2, Huma Naz^1,2

¹Department of Medicine-Endocrinology and Metabolism, University of Missouri School of Medicine, Columbia, Missouri, United States.

American journal of physiology. Endocrinology and metabolism

|August 28, 2024

概括

内皮细胞特异性CD36 (ECCD36) 信号驱动西方饮食诱导的脂质乱和骨肌肉中的胰岛素抵抗. 阻止ECCD36可以改善新陈代谢健康,并减轻饮食引起的肌肉功能障碍.

科学领域:

代谢和心血管疾病
分子和细胞生物学分子和细胞生物学

背景情况:

西方饮食 (WD) 促进CD36表达,导致脂质代谢障碍和胰岛素抵抗.
内皮细胞特异性CD36 (ECCD36) 在骨肌肉功能障碍中的作用尚未完全理解.

研究的目的:

研究ECCD36在骨肌肉脂质代谢,胰岛素抵抗和线粒体功能中的作用.
阐明由ECCD36.6调解的WD诱导的骨肌异常背后的分子机制.

主要方法:

使用的雌性野生型 (ECCD36+/+) 和淘汰型 (ECCD36-/-) 老鼠,在16周内食WD或标准.
评估了代谢参数,胰岛素敏感性,葡萄糖吸收和骨肌肉脂质积累.
在实验室中研究了棕酸诱导的脂质积累在内皮细胞 (ECs).

主要成果:

与WD的野生类型小鼠相比,ECCD36淘汰赛小鼠表现出更好的胰岛素敏感性,葡萄糖耐受性和减弱的脂质积累.
ECCD36缺乏减少了WD诱导的自由脂肪酸 (FFA) 吸收,宫外脂质积累和骨肌中的线粒体功能障碍.
实验室研究表明,ECCD36在EC中调解棕酸诱导的脂质积累,释放FFAs.

结论:

内皮特异性CD36信号传递是WD诱导的骨肌脂代谢障碍和胰岛素抵抗的关键调解者.
通过促进FFA吸收,脂质积累和线粒体功能障碍,ECCD36有助于骨肌肉功能障碍.
准ECCD36可能为饮食引起的肥胖和相关的代谢并发症提供治疗策略.

关键词:

CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 内皮细胞是内皮细胞.胰岛素耐药性是一种胰岛素耐药性.肥胖肥胖肥胖肥胖肥胖肥胖肥胖肥胖这是骨肌肉的骨架肌肉.

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