肠道微生物群衍生代谢物英多尔-3-酸通过向STAT3来对抗饮食诱导的肥胖症来增强瘦素敏感性
Zhiwei Wang1, Shaying Yang1, Liangju Liu1
1Department of Pharmacology, Wuxi School of Medicine, Jiangnan University, Wuxi, China.
Clinical and translational medicine
|November 28, 2024
概括
肠道细菌的代谢物英多尔-3-酸 (IPA) 通过使身体对勒素敏感来抵消肥胖. 补充IPA或Clostridia细菌显示出治疗肥胖和改善代谢健康的前景.
科学领域:
- 微生物学 微生物学
- 代谢过程中的代谢.
- 神经内分泌学神经内分泌学
背景情况:
- 肥胖与肠道微生物组的改变有关.
- 肠道微生物组产生会影响宿主生理学的代谢物.
- 瘦素抵抗是肥胖发展的关键因素.
研究的目的:
- 研究肠道共生细菌在调节宿主能量平衡中的作用.
- 为了识别与肥胖有关的微生物代谢物.
- 探索微生物组衍生代谢物对肥胖的治疗潜力.
主要方法:
- 在小鼠模型中研究了 indole-3-propionic acid (IPA) 对宿主代谢的影响.
- 利用体外拉下测试和局部定向突变发生法来识别分子相互作用.
- 给饮食引起的肥胖 (DIO) 和肥胖小鼠服用IPA和Clostridium Sporogenes.
主要成果:
- 来自Clostridia的托芬代谢物IPA通过向下丘脑的STAT3.3来使宿主对瘦素敏感.
- 高脂肪饮食会减少肠道内菌和IPA的产生.
- IPA补充剂或Clostridium sporogenes的使用改善了DIO小鼠的新陈代谢参数,但不是没有勒的小鼠.
结论:
- 由IPA介导的肠-大脑轴调节宿主新陈代谢,并对抗肥胖.
- IPA作为一种内源性瘦素敏感剂.
- 来自微生物组的IPA补充剂代表了对肥胖的潜在治疗策略.
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