高糖饮食诱导的血氧利平特征反映了肠道屏障功能障碍的饮食风险
Qing-Jin Pan1,2,3, Hou-Hua Yin1,2,3, Ya-Nan Liu1,2,3
1CNTTI of College of Pharmacy & Anesthesia Department of the Second Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China.
Journal of agricultural and food chemistry
|August 28, 2025
概括
高糖饮食改变了血氧利平,增加了8~9) - 环氧酸 (8~9) - EET. 这种代谢物可能表明肠道屏障受损和过度摄入糖的代谢压力.
科学领域:
- 代谢学
- 肠道健康
- 饮食影响
背景情况:
- 高糖饮食 (HSD) 影响结肠氧利平,导致肠道屏障功能障碍.
- 由于HSD而导致的全身氧利平特征变化及其与肠道屏障损害的联系尚不清楚.
研究的目的:
- 研究HSD对血氧利平的作用.
- 确定血氧利平是否可以作为HSD诱导的肠道屏障损伤的生物标志物.
主要方法:
- 在给HSD养的小鼠模型中分析血氧利平的概况.
- 特定氧利平与肠道屏障标记物的相关性分析 (脂多糖).
- 与常规高糖摄入量的人群与对照人群的血氧利平概况比较.
主要成果:
- HSD显著改变了血氧利平的代谢,特别是CYP环氧酶途径的代谢物.
- 在小鼠中,血8(9) - 环氧松酸 (8(9) - EET增加了2. 4倍,在人类中增加了3. 7倍.
- 在小鼠和人类中,高8~9) - EET与肠道功能障碍和脂多糖水平呈正相关性.
结论:
- HSD重编程了血氧利平的概况,其关键发现是8~9) -EET升高.
- 增加的8~9) -EET可能表明代谢压力,并作为饮食糖过载的早期指标.
- 血氧利平分析,特别是8(9)-EET,为评估HSD引起的肠损伤风险提供了一个潜在的工具.
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