肠道微生物群和衍生代谢物 中介 阻塞性睡眠呼吸暂停 诱导动脉样硬化
bioRxiv : the preprint server for biology
|November 28, 2024
概括
阻塞性睡眠呼吸暂停 (OSA) 与间歇性缺氧/高头 (IHC) 恶化动脉样硬化,特别是在大动脉,通过改变肠道微生物群和胆汁酸. 没有细菌的小鼠表现出降低了动脉样硬化,突出显示了肠道微生物群.
科学领域:
- 微生物组研究的研究.
- 心血管疾病是什么心血管疾病
- 代谢学 代谢学 代谢学
背景情况:
- 阻塞性睡眠呼吸暂停 (OSA) 与间歇性缺氧/超 (IHC) 和增加动脉样硬化风险有关,特别是在肥胖个体中.
- 肠道微生物群和代谢物参与动脉动脉生成,促使人们对其在OSA诱导的动脉样硬化中的作用进行调查.
研究的目的:
- 研究肠道微生物群和代谢物对在模仿阻塞性睡眠呼吸暂停 (OSA) 的条件下动脉样硬化发展的贡献.
- 为了比较没有细菌的动脉样硬化与常规养殖的小鼠,这些小鼠被暴露在高脂肪,高胆固醇饮食和间歇性缺氧/高头症 (IHC) 中.
主要方法:
- 使用无细菌 (GF) 和无特定病原体 (SPF) 的ApoE-/-小鼠在高脂肪,高胆固醇 (HFHC) 饮食中,有或没有间歇性缺氧/高头 (IHC).
- 使用16S rRNA基因测序分析便微生物群和使用液体染色学-并联质谱法 (LC-MS/MS) 分析代谢组.
- 在大动脉和肺动脉 (PA) 中量化动脉样硬化病变.
主要成果:
- 高脂肪,高胆固醇饮食 (HFHC) 在SPF小鼠中显著增加了动脉样硬化;IHC加剧了这些病变.
- 肠道微生物群分析显示,在HFHC-IHC组中,Akkermansiaceae的丰富和Muribaculaceae的枯竭.
- 无细菌 (GF) ApoE-/-小鼠在HFHC/IHC条件下与SPF小鼠相比显著减少了大动脉动脉样硬化,而PA动脉样硬化不受微生物殖民的影响.
结论:
- 间歇性缺氧/超 (IHC) 和高脂肪,高胆固醇饮食 (HFHC) 协同促进动脉样硬化,主要在主动脉中,由肠道微生物群介导.
- 在Akkermansiaceae和Muribaculaceae中的特定不平衡,以及改变的胆酸特征 (例如,脱氧胆酸),是OSA诱导的大动脉动脉样硬化的关键因素.
- 这些发现为预防和治疗与阻塞性睡眠呼吸暂停 (OSA) 相关的动脉样硬化提供了新的治疗点.
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