冠状动脉体缩改善了肥胖小鼠的高血糖
Mi-Kyung Shin1, Wan-Yee Tang2, Mateus R Amorim1
1Department of Anesthesiology and Critical Care Medicine, George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, United States.
Journal of applied physiology (Bethesda, Md. : 1985)
|December 21, 2023
概括
在肥胖小鼠中,状体变色会降低高血压,并通过影响肝脏葡萄糖,而不是胰岛素抵抗,改善葡萄糖水平. 针对心血管内特定受体的遗传向并没有改变葡萄糖代谢.
科学领域:
- 生理学 生理学 生理学
- 代谢研究研究 代谢研究
- 内分泌学 在内分泌学.
背景情况:
- 动脉体 (CBs) 涉及与肥胖相关的葡萄糖异常,可能是通过交感神经系统的激活.
- 肥胖引起的高血压涉及胰岛素受体 (INSR) 和瘦素受体 (LEPR) 在CB中的信号,激活TRPM7.
研究的目的:
- 为了调查心动脉体缩 (CSND) 或CB中的Lepr,Trpm7和Insr的基因淘汰是否会减轻饮食诱导的肥胖 (DIO) 小鼠的高血糖症,葡萄糖不耐受性和胰岛素耐药性.
主要方法:
- 对75只雄性DIO小鼠进行了实验,涉及CSND (vs.假) 或shRNA诱导的基因抑制在CB.
- 测量包括血压遥测,葡萄糖和胰岛素耐受性测试,以及激素的血/肝分析,葡萄糖代谢标志物和基因表达.
主要成果:
- 在不影响胰岛素抵抗的情况下,CSND显著降低了血压,禁食血糖,并改善了葡萄糖耐受性.
- CSND导致肝脏糖原水平增加,但没有改变激素水平或葡萄糖生成酶表达.
- 在CB中,Lepr,Trpm7或Insr的遗传淘汰对葡萄糖代谢没有影响.
结论:
- 动脉体有助于与肥胖相关的高血糖症,可能是通过调节糖原-葡萄糖平衡.
- 肥胖对小鼠CB的糖尿病效应似乎不涉及CBLepr,Trpm7和Insr的激活.
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