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肠道微生物群和衍生代谢物介导阻塞性睡眠呼吸暂停诱导动脉样硬化

Jin Xue¹, Celeste Allaband¹, Simone Zuffa^2,3

¹Department of Pediatrics, University of California San Diego, La Jolla, CA, USA.

|March 3, 2025

概括

阻塞性睡眠呼吸暂停 (OSA) 与间歇性缺氧/超 (IHC) 会使动脉样硬化恶化,特别是在大动脉中. 受饮食影响的肠道微生物群和胆汁酸在这个过程中发挥着关键作用,提供了潜在的治疗点.

科学领域:

心血管研究研究心血管研究
微生物组研究微生物组研究
代谢学代谢学代谢学

背景情况:

阻塞性睡眠呼吸暂停 (OSA) 与动脉样硬化风险增加有关,这种风险是由间歇性缺氧/超症 (IHC) 驱动的.
肠道微生物群及其代谢物与动脉动脉生成有关,但它们在OSA诱导的动脉样硬化中的具体作用尚不清楚.

研究的目的:

研究肠道微生物群和代谢物对动脉样硬化发展的贡献,在模仿OSA (IHC) 和高脂肪,高胆固醇饮食 (HFHC) 的条件下.
在这些条件下,比较无细菌 (GF) 和无特定病原体 (SPF) 的小鼠中的动脉样硬化进展.

主要方法:

Apoe-/-小鼠被食高脂肪,高胆固醇 (HFHC) 饮食或定期食 (RC),经过间歇性缺氧/高头 (IHC) 或正常氧.
使用16S rRNA基因测序分析了便微生物群组成.
使用非向的双重质谱法 (LC-MS/MS) 进行了代谢分析.

主要成果:

HFHC饮食显著增加了SPF小鼠的大动脉和肺动脉 (PA) 的动脉样硬化.
在HFHC饮食之外,IHC加剧了动脉样硬化.
与HFHC/IHC条件下的SPF小鼠相比,GF小鼠的动脉动脉样硬化减少,这表明肠道微生物群的作用.
特定的肠道细菌 (Akkermansiaceae丰富,Muribaculaceae枯竭) 和胆酸失调 (例如,脱氧醇酸) 与动脉样硬化有关.

结论:

间歇性缺氧/高头和高脂肪,高胆固醇饮食协同促进动脉样硬化,特别是在大动脉.
肠道微生物群显著调节饮食和IHC诱导的大动脉动脉样硬化,但不是肺动脉动脉样硬化.
特定肠道细菌家族的不平衡和改变的胆酸概况是OSA相关动脉样硬化的关键媒介,这表明了新的治疗点.

关键词:

动脉样硬化是一种动脉样硬化.饮食饮食饮食饮食没有细菌,没有细菌.间歇性的缺氧/高头.我们的微生物群.

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