肥胖促进了富蒙尼辛B1肝毒性
Léonie Dopavogui1, Marion Régnier1, Arnaud Polizzi1
1Toxalim (Research Centre in Food Toxicology), Université de Toulouse, INRAE, ENVT, INP-Purpan, UPS, Toulouse, France.
The Science of the total environment
|May 29, 2023
概括
肥胖会加剧肝脏炎症和肠道失调,当暴露于食物污染物fumonisin B1 (FB1) 时. 这项研究揭示了肥胖引起的肝炎与小鼠的FB1暴露有关.
科学领域:
- 毒理学 毒理学 毒理学
- 代谢性疾病是一种代谢性疾病.
- 胃肠病学 胃肠病学
背景情况:
- 肥胖是一个全球性的健康问题,与慢性炎症和代谢并发症有关.
- 食物污染物,如米尼辛B1 (FB1),一种真菌毒素,可能与与肥胖有关的健康问题相互作用.
- 肥胖对菌根毒素,特别是FB1的敏感性,肠道健康和肝脏毒性的影响尚不清楚.
研究的目的:
- 调查饮食诱导的肥胖是否调节了对口服富蒙尼辛B1 (FB1) 暴露的敏感性.
- 评估FB1对肠道健康和肥胖和非肥胖小鼠肝毒性的影响.
- 探索高脂肪饮食 (HFD) 和FB1暴露的代谢和炎症后果.
主要方法:
- 雄性C57BL/6J小鼠被食高脂肪饮食 (HFD) 或正常食 (CHOW) 15周.
- 在最后的3周内,小鼠通过饮用水获得FB1 (10毫克/公斤/天),与各自的饮食一起.
- 评估的参数包括体重,禁食葡萄糖,肝硬化,肠道微生物群,血FB1水平,肝酶和基因表达.
主要成果:
- HFD诱导肥胖,高血糖和肝硬化. 结合HFD和FB1暴露导致体重减轻,禁食葡萄糖降低,肠道失调,血FB1增加.
- HFD/FB1治疗显著增加了血中氨基酶,表明肝损伤,并增加了肝炎.
- 基因表达分析显示,HFD/FB1治疗小鼠的脂质生成减少,免疫反应增加和细胞循环基因增加.
结论:
- 肥胖会增强富蒙尼辛B1 (FB1) 的不良影响,促进肠道失调和严重的肝炎.
- 这项研究提供了首次证据,表明肥胖引起的肝炎是由于接触常见的食品污染物的结果.
- 这些发现突出了代谢状态和食品污染物毒性之间的关键相互作用,强调了公共卫生问题.
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