微血管胰岛素抵抗与CD36缺乏症中肌肉葡萄糖处理的增强有关
Cyndya Shibao1, Vivek S Peche2, Ian M Williams3
1Department of Medicine, Division of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville TN.
medRxiv : the preprint server for health sciences
|February 26, 2024
概括
减少CD36表达改善了小鼠和人类的葡萄糖处理,尽管引起了微血管功能障碍. 这表明CD36缺乏矛盾地通过肌肉基因表达变化提高葡萄糖利用率.
科学领域:
- 内分泌学 在内分泌学.
- 血管生物学 血管生物学
- 代谢研究研究 代谢研究
背景情况:
- 肌肉内皮胰岛素的输送对代谢调节至关重要.
- 脂肪酸载体CD36存在于内皮细胞中,并影响胰岛素信号传递.
- 遗传的CD36缺乏导致内皮功能障碍,但其与胰岛素抵抗的联系尚未完全理解.
研究的目的:
- 为了研究CD36缺乏和胰岛素抵抗之间的关联.
- 为了确定减少CD36表达对葡萄糖代谢和微血管功能的影响.
主要方法:
- 在CD36缺乏和野生型小鼠中进行了高胰岛素/高血糖.
- 研究对50%的CD36缺乏的人进行了研究,并与对照对照进行了匹配.
- 人类微血管细胞中的CD36敲击评估了胰岛素信号通路.
主要成果:
- 缺乏CD36的小鼠表现出增强的全身葡萄糖排放.
- 与对照组相比,部分CD36缺乏的人类显示葡萄糖处置有所改善.
- CD36敲击损害了胰岛素对AKT,eNOS和微血管细胞中氧化释放的作用.
结论:
- 矛盾的是,CD36缺乏与葡萄糖利用率的增加有关,尽管微血管胰岛素抵抗.
- 在CD36缺乏症中,增强的葡萄糖排放可能是肌肉基因表达重塑的结果.
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