胰岛素导致人体内皮质功能障碍:部位和机制
Guido Arcaro1, Anna Cretti, Sara Balzano
1Division of Endocrinology, Department of Biomedical and Surgical Sciences, University of Verona Medical School and Azienda Ospedaliera di Verona, Verona, Italy.
高水平的胰岛素通过减少内皮依赖的血管扩张来损害血管功能,这可能是由于氧化应激增加. 这一发现将胰岛素抵抗与动脉样硬化联系在一起.
科学领域:
- 心血管生理学心血管生理学
- 内分泌学 在内分泌学.
- 血管生物学 血管生物学
背景情况:
- 胰岛素耐药性和高胰岛素血症与动脉样硬化有关.
- 内皮在动脉生成中起着至关重要的作用.
- 在体内,高胰岛素血症对大动脉内皮功能的影响尚不清楚.
研究的目的:
- 为了研究高胰岛素血症对大导管动脉内皮功能的体内影响.
- 为了确定高胰岛素血症是否会损害内皮依赖的血管扩张.
- 探索氧化应激在胰岛素诱导的内皮功能障碍中的作用.
主要方法:
- 健康的受试者接受了低血糖胰岛素在低和高生理度.
- 使用回声多普勒评估了内皮依赖 (流媒体) 和独立 (尼甘油诱导) 血管扩张.
- 评估了抗氧化剂 (维生素C) 输注对胰岛素诱导的内皮变化的影响.
主要成果:
- 低和高的生理超胰岛素血症都消除了大动脉中依赖内皮细胞的血管扩张.
- 内皮独立的血管扩张没有受到高胰岛素血的影响.
- 服用维生素C完全恢复了因胰岛素受损的内皮功能.
结论:
- 温和的胰岛素高血压,类似于胰岛素抵抗的禁食水平,会损害大动脉内皮依赖的大血管扩张.
- 增加的氧化应激是这种内皮功能障碍背后的可能机制.
- 这些发现为高胰岛素血症/胰岛素耐药性和人类动脉样硬化之间提供了病理生理学联系.
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