高脂肪饮食诱导的结肠细胞功能障碍升级微生物衍生的三甲氧化物
Woongjae Yoo1,2, Jacob K Zieba1,2, Nora J Foegeding2,2
1Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
概括
一种高脂肪饮食会改变肠道细菌
科学领域:
- 微生物学
- 肠道微生物组
- 代谢疾病
背景情况:
- 西方高胆饮食通过肠道微生物代谢促进心血管疾病.
- 胆转化为三甲基胺 (TMA),这是有害代谢物的前体.
- 饮食引起的肠道生理变化对微生物代谢的影响尚不清楚.
研究的目的:
- 研究高脂肪饮食如何改变肠道生理.
- 确定这些变化是否影响肠道微生物的胆代谢.
- 将这些变化与心血管疾病风险联系起来.
主要方法:
- 使用一种由饮食引起的肥胖小鼠模型.
- 分析了结肠上皮线粒体的生物能量.
- 在肠道光中测量氧和酸盐的生物可用性.
- 评估了大肠杆菌的胆代谢
- 量化循环中的三甲基胺N氧化物 (TMAO) 含量.
主要成果:
- 高脂肪饮食导致结肠上皮层线粒体功能受损.
- 这导致光线氧和酸盐的可用性增加.
- 增加了其依赖呼吸的胆代谢.
- 循环中的TMAO水平升高.
结论:
- 饮食引起的肠道生理变化可以提高肠道微生物的新陈代谢.
- 高脂肪饮食通过增加大肠杆菌胆代谢促进TMAO的产生.
- 这种机制将西方饮食与心血管疾病的风险联系在一起.
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