迪铁素通过改变肠道微生物群和LPS/TLR4/NF-κB炎症通路,加剧肥胖小鼠的肝脏胰岛素抵抗
Yin-Yi Ding1,2, Jinchi Lan1, Yumeng Fang1
1Food Safety Key Laboratory of Zhejiang Province, Food Nutrition Science Centre, School of Food Science and Biotechnology, Zhejiang Gongshang University, Hangzhou, 310018, China.
Molecular nutrition & food research
|September 19, 2023
概括
蛋白质氧化产物迪铁因,通过破坏肠道微生物群并触发炎症反应,使胰岛素抵抗恶化,特别是在高脂肪饮食养的小鼠中.
科学领域:
- 生物化学 生化学
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
背景情况:
- 迪铁是蛋白质氧化的主要产物,并对健康构成风险.
- 胰岛素抵抗是与各种因素相关的日益严重的健康问题.
研究的目的:
- 为了调查dityrosine是否会加剧胰岛素耐药性.
- 为了确定迪蒂罗辛是否会诱导肠道菌群的干扰和炎症.
主要方法:
- 给小鼠提供正常或高脂肪饮食,并给小鼠提供13周的迪蒂罗辛或盐水.
- 试管发酵评估了从不同小鼠模型中对肠道微生物群的dityrosine的影响.
- 测量了炎症和胰岛素敏感性的血生物标志物.
主要成果:
- 在正常饮食小鼠中,迪提洛辛诱导了胰岛素抵抗,在高脂肪饮食小鼠中,它使其恶化.
- 迪铁素改变了肠道微生物群的组成,增加了炎症标志物 (LPS,LBP,TLR4,NF-κB,TNF-α,IL-6,IL-8),同时降低了IL-10.
- 肠道菌群的变化与炎症生物标志物的改变相关.
结论:
- 迪蒂洛辛对胰岛素耐药性的影响与肠道微生物群的变化有关.
- 迪铁素促进LPS/TLR4/NF-κB炎症通路,有助于胰岛素抵抗,特别是在肥胖症中.
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