国际生殖健康/计划生育杂志 ›› 2026, Vol. 45 ›› Issue (5): 429-433.doi: 10.12280/gjszjk.20260223

• 综述 • 上一篇    下一篇

拟杆菌门相关菌群参与多囊卵巢综合征发病的代谢机制及靶向干预进展

樊妍侗, 刘芳,△(), 王硕荣, 赵书冉, 王志敏, 原源   

  1. 010050 呼和浩特, 内蒙古医科大学(樊妍侗,王硕荣,赵书冉);内蒙古医科大学附属医院(刘芳, 王志敏, 原源)
  • 收稿日期:2026-04-24 出版日期:2026-09-15 发布日期:2026-09-20
  • 通讯作者: 刘芳,E-mail:13015005798@163.com
  • 作者简介:△审校者
  • 基金资助:
    内蒙古医科大学面上项目(YKD2025MS004);国家自然科学基金项目(地区科学基金项目)(82460171)

Bacteroidetes-Related Gut Microbiota in the Pathogenesis of Polycystic Ovary Syndrome: Metabolic Mechanisms and Targeted Interventions

FAN Yan-tong, LIU Fang,△(), WANG Shuo-rong, ZHAO Shu-ran, WANG Zhi-min, YUAN Yuan   

  1. Inner Mongolia Medical University, Hohhot 010050, China (FAN Yan-tong, WANG Shuo-rong, ZHAO Shu-ran); The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010050, China (LIU Fang, WANG Zhi-min, YUAN Yuan)
  • Received:2026-04-24 Published:2026-09-15 Online:2026-09-20
  • Contact: LIU Fang, E-mail: 13015005798@163.com

摘要:

近年来,肠道菌群在多囊卵巢综合征(polycystic ovary syndrome,PCOS)发生发展中的作用备受关注,其中拟杆菌门相关菌群(Bacteroidetes-related gut microbiota)的丰度改变可能与PCOS的临床特征相关。拟杆菌门相关菌群可通过胆盐水解酶(bile salt hydrolase,BSH)水解初级胆汁酸,下调肠道法尼酯X受体(farnesoid X receptor,FXR)信号;亦可通过代谢物胍丁胺以非胆汁酸依赖方式激活FXR,抑制胰高血糖素样肽1(glucagon-like peptide 1,GLP-1)分泌;还可经脂多糖(lipopolysaccharide,LPS)介导的慢性炎症诱发胰岛素抵抗。在治疗方面,以益生菌/合生元为代表的肠道菌群干预策略已在PCOS患者中展现出改善代谢指标的潜力,但针对拟杆菌门相关菌群的精准干预策略仍有待进一步研究。深入阐明拟杆菌门相关菌群-PCOS代谢通路可能为PCOS的精准治疗提供新的靶点。

关键词: 多囊卵巢综合征, 拟杆菌门, 胃肠道微生物组, 胆汁酸代谢, 法尼醇X受体, 胰高血糖素样肽1

Abstract:

In recent years, increasing attention has been paid to the role of gut microbiota in the development and progression of polycystic ovary syndrome (PCOS), among which the altered abundance of Bacteroidetes-related gut microbiota may be related to the clinical characteristics of PCOS. Bacteroidetes-related gut microbiota may hydrolyze primary bile acids via bile salt hydrolase (BSH), thereby downregulating intestinal farnesoid X receptor (FXR) signaling; it may also activate FXR in a bile acid-independent manner through its metabolite agmatine, inhibiting glucagon-like peptide 1 (GLP-1) secretion; furthermore, it may induce insulin resistance via lipopolysaccharide (LPS)-mediated chronic inflammation. In terms of therapeutic interventions, the gut microbiota modulation strategy represented by probiotics/synbiotics has shown potential in improving metabolic parameters in patients with PCOS. However, the precision intervention strategies targeting Bacteroidetes-related gut microbiota remain to be further investigated. Elucidating the Bacteroidetes-PCOS metabolic pathways may provide new targets for the precise treatment of PCOS.

Key words: Polycystic ovary syndrome, Bacteroidetes, Gastrointestinal microbiome, Bile acid metabolism, Farnesoid X receptor, Glucagon-like peptide 1