氨酸的限制通过增加奥西利巴克特杂媒介的托调节来减轻与肥胖相关的焦虑类行为
Feng Zhao1,2, Jiao Wang1,2, Weijuan Liang1,2
1Department of Health Laboratory Technology, School of Public Health, Chongqing Medical University, Chongqing, 400016, People's Republic of China.
Microbiome
|November 29, 2025
概括
素限制饮食 (LRD) 通过改变肠道细菌和增强托,一种向FTO-IGF2BP1-LGR6通路的代谢物,减少肥胖症中类似焦虑的行为.
科学领域:
- 神经科学是一个神经科学.
- 微生物学 微生物学
- 代谢科学 代谢科学
背景情况:
- 与肥胖相关的焦虑是一个日益关注的问题.
- 饮食干预措施,如素限制饮食 (LRD),显示出潜力,但机制尚不清楚.
- 肠道微生物群-代谢物-大脑轴在LRD的影响中的作用尚不清楚.
研究的目的:
- 调查LRD对肥胖症焦虑类行为的影响.
- 阐明肠道微生物群及其代谢物在LRD治疗作用中的作用.
- 为了确定涉及LRD作用的分子通路.
主要方法:
- 在动物中利用高脂肪饮食 (HFD) 诱导肥胖和慢性克制压力模型.
- 服用素限制饮食 (LRD) 和奥西利巴克特类动物 (有活力和封装).
- 分析了肠道微生物群的组成,代谢物水平 (托),肠道屏障功能和分子信号通路 (FTO-IGF2BP1-LGR6).
主要成果:
- 在HFD养的动物中,LRD减轻了类似焦虑的行为,减轻了体重,并改善了葡萄糖代谢.
- LRD显著改变了肠道微生物群,增加了杆菌的丰富性.
- 托醇是Oscillibacter ruminantium的代谢物,通过抑制FTO介导的IGF2BP1和减少Lgr6mRNA的m6A修饰来逆转类似焦虑的行为.
结论:
- 通过丰富Oscillibacter反动物和调节托生产,LRD可以改善与肥胖相关的焦虑.
- FTO-IGF2BP1-LGR6信号轴是中介LRD抗焦虑作用的关键途径.
- LRD代表了一种有前途的微生物群导向治疗策略,用于与代谢压力相关的神经行为障碍.
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