帕拉巴克特罗伊德斯 (Parabacteroides distasonis) 通过激活肠道GPR109a改善了胰岛素耐药性
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Updated: Jul 10, 2025

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Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
Published on: November 16, 2011
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Yonggan Sun1,2,3, Qixing Nie1,2,3, Shanshan Zhang1,2,3
1State Key Laboratory of Food Science and Resources, Nanchang University, Nanchang, China.
Nature communications
|November 25, 2023
概括
帕巴克特罗伊德斯 distasonis 通过增强肠道屏障功能和减少炎症,有利于胰岛素抵抗 (IR). 它的衍生品尼古丁酸 (NA) 和食纤维Dendrobium officinale多糖 (DOP) 提供潜在的IR治疗策略.
科学领域:
- 微生物学 微生物学
- 代谢疾病 代谢疾病
- 免疫学 免疫学 免疫学
背景情况:
- 肠道微生物群显著影响代谢健康,特别是胰岛素抵抗 (IR).
- 特定的细菌物种及其代谢物越来越多地被认为是它们在IR病原发生中的作用.
- 了解这些微生物的贡献对于开发新的治疗干预措施至关重要.
研究的目的:
- 研究中国成年人肠道微生物群组成与胰岛素抵抗之间的关联.
- 为了确定特定的细菌物种及其代谢物,可以改善胰岛素抵抗.
- 探索饮食干预措施来调节有益的肠道细菌并预防胰岛素抵抗.
主要方法:
- 对中国成年人进行的病例对照研究 (ChiCTR2200065715),以将肠道微生物群与IR相关联.
- 使用小鼠模型进行体内研究,以评估Parabacteroides distasonis及其代谢物对IR的影响.
- 对生物活性食纤维进行查,以检测其促进P. distasonis生长和改善IR的能力.
- 在一个单独的人类队列中验证发现,患者患有2型糖尿病.
主要成果:
- 研究人员发现,Parabacteroides distasonis与胰岛素耐药性相反相关.
- 用P. distasonis治疗改善了胰岛素抵抗,增强了肠道完整性,并减少了小鼠的全身炎症.
- 从P. distasonis衍生出的尼古丁酸 (NA) 被确定为通过激活GPR109a来加强肠道屏障的关键分子,从而改善IR.
- 丹德罗 officinale 多糖 (DOP) 促进了P. distasonis的生长,并对小鼠的IR进行了保护.
- 在人类2型糖尿病队列中证实了P. distasonis和NA的降低水平.
结论:
- 帕拉巴克特罗伊德 (Parabacteroides distasonis) 通过其衍生的尼古丁酸在抗胰岛素抵抗方面起着保护作用.
- 通过NA激活肠道GPR109a通路是改善胰岛素抵抗的关键机制.
- 生物活性食纤维,如DOP,可用于促进有益的肠道细菌,如P. distasonis用于IR预防和治疗.
- 这些发现为通过肠道微生物群调节来管理胰岛素抵抗提供了有希望的策略.
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