周血管脂肪发出的"血管"信号:一种将胰岛素抵抗与血管疾病联系起来的机制
John S Yudkin1, Etto Eringa, Coen D A Stehouwer
1Diabetes and Cardiovascular Disease Academic Unit, Department of Medicine, Royal Free and University College Medical School, The Archway Campus, Holborn Union Building, 2-10 Highgate Hill, London N19 5LW, UK. j.yudkin@ucl.ac.uk
Lancet (London, England)
|May 25, 2005
概括
肥胖会损害胰岛素的血管作用,原因是脂肪沉积会释放瘤缩因子α. 这会导致血管收缩,阻碍胰岛素扩大血管的能力.
科学领域:
- 身体生理学 身体生理学
- 内分泌学 在内分泌学.
- 血管生物学 血管生物学
背景情况:
- 脂肪组织释放细胞因子,影响肝脏和肌肉中的胰岛素信号传递.
- 肥胖与胰岛素介导血管扩张受损有关.
- 动脉附近的局部脂肪沉积可能起到血管调节作用.
研究的目的:
- 为了研究骨肌动脉小动脉中周动脉脂肪的血管调节作用.
- 阐明胰岛素介导血管扩张和血管收缩的机制.
- 探索肥胖对这些血管反应的影响.
主要方法:
- 从老鼠的肌肉中分离出第一阶段的动脉小动脉.
- 评估胰岛素对内甲素-1和氧化 (NO) 途径的影响.
- 对肥胖大鼠动脉中阿迪波基因 (瘤亡因子α) 的参与进行分析.
主要成果:
- 胰岛素具有双重调节作用:内甲素-1介导的血管收缩和NO介导的血管扩张.
- 肥胖大鼠的动脉小关节显示胰岛素刺激的NO合成受损,导致无阻抗的血管收缩.
- 周动脉脂肪中的瘤缩因子α与这种受损血管扩张有关.
结论:
- 在肥胖中,周动脉脂肪储存产生瘤亡因子α,导致血管收缩.
- 这种细胞因子的"血清"信号抑制了胰岛素介导的毛细血管招募.
- 这种机制可能会将内脏脂肪,胰岛素抵抗和血管疾病联系起来.
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