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普雷沃特拉·科普里 (Prevotella copri) 促进了白色脂肪的色化,并改善了脂肪的状况

Shuang Liu¹, Haifang Li², Rui Li³

¹College of Animal Science and Technology, Shandong Agricultural University, Tai'an, People's Republic of China.

Nature communications

|December 13, 2025

概括

在肥胖患者中,Prevotella copri的丰度较低. 这种肠道细菌及其代谢物酸盐促进白色脂肪组织的色,为抗肥胖提供潜在的策略.

科学领域:

微生物组研究的研究.
代谢性疾病研究研究.
脂肪组织生物学脂肪组织生物学

背景情况:

肠道微生物群共生体Prevotella对其在宿主健康中的作用知之甚少.
在新陈代谢调节中Prevotella copri的特定功能尚不清楚.

研究的目的:

研究Prevotella copri在肥胖和脂肪组织代谢中的作用.
确定P. copri影响宿主代谢健康的机制.

主要方法:

对一个患有肥胖症的中国队列的病例控制分析.
高脂肪饮食 (HFD) 诱导脂肪的小鼠模型.
代谢分析以确定关键代谢物.
分子生物学技术用于阐明信号通路 (IL-6-STAT3,FOXM1).

主要成果:

在肥胖患者中观察到较低的便Prevotella copri丰度.
在HFD诱导的肥胖小鼠中,P. copri的使用缓解了脂肪沉积,并促进了 inguinal 白脂肪组织 (iWAT) 的棕色化.
苏酸盐被确定为通过SUCNR1激活调解P.copri效应的关键代谢物.
增加iWAT巨细胞群和IL-6-STAT3通路激活在P.copri或苏酸盐治疗中观察到.
发现FOXM1可以对IL-6进行上调,从而激活iWAT棕色化中的IL-6-STAT3通路.
在人类WAT中,P.copri,酸盐水平和TBX1/UCP1转录之间存在正相关性.

结论:

普雷沃特拉·科普里 (Prevotella copri) 在促进iWAT棕色化方面发挥着重要作用.
苏酸盐作为一种关键的P. copri衍生代谢物,影响脂肪组织.
IL-6-STAT3和FOXM1通路参与了P.copri介导的iWAT棕色化.
研究结果表明,针对P.copri或苏酸盐的潜在治疗策略可用于肥胖管理.

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