慢性间歇性缺氧诱导的消化不良与肝氧化压力,线粒体功能障碍和炎症有关
Joana L Fernandes1, Fátima O Martins1, Elena Olea2,3
1iNOVA4Health, NOVA Medical School, Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, 1150-069 Lisboa, Portugal.
Antioxidants (Basel, Switzerland)
|November 25, 2023
概括
阻塞性睡眠呼吸暂停 (OSA) 导致肝脏功能障碍,导致代谢障碍. 慢性间歇性缺氧 (CIH) 在OSA中损害肝脏线粒体,增加氧化应激,导致代谢不良.
科学领域:
- 肝病学 肝病学是一种肝病学.
- 代谢障碍 代谢障碍 代谢障碍
- 睡眠医学 睡眠医学
背景情况:
- 阻塞性睡眠呼吸暂停 (OSA) 与代谢障碍有关,但机制尚不清楚.
- 肝脏在代谢平衡中的作用表明,它是OSA相关功能障碍的关键.
- 这项研究研究了与OSA相关的代谢问题中的肝功能障碍机制.
研究的目的:
- 探索肝功能障碍在与OSA相关的代谢功能障碍中的作用.
- 阐明将OSA和肝脏内的代谢障碍联系在一起的分子机制.
主要方法:
- 雄性Wistar大鼠被食控制或高脂肪 (HF) 饮食12周.
- 慢性间歇性缺氧 (CIH),模仿OSA,在过去15天内被应用.
- 分析了肝脏组织的脂质沉积,胰岛素信号,氧化应激,线粒体功能和炎症.
主要成果:
- 两种CIH和HF饮食都诱导了代谢不良;HF饮食+CIH并没有使这种情况恶化.
- 在肥胖大鼠中,CIH加剧了肝脂沉积.
- CIH降低了氧化酸化复合物和SOD-1;HF饮食降低了线粒体密度和抗氧化能力.
- 这两种刺激都改变了硫醇水平,增加了促炎性标志物.
结论:
- 肝脏线粒体功能障碍和氧化应激有助于与OSA相关的代谢障碍.
- 炎症是与OSA相关的代谢功能障碍发展的一个重要因素.
- 肝功能障碍是OSA和代谢障碍之间的关键联系.
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