1.汕头大学医学院,广东 汕头 515000
2.汕头大学医学院第一附属医院,广东 汕头 515000
林康毅,第一作者,研究方向:肠道菌群与多囊卵巢综合征,E-mail: 21kylin@stu.edu.cn
收稿:2025-02-27,
修回:2025-06-03,
录用:2025-07-03,
纸质出版:2025-09-20
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林康毅,鄞国书.肠道菌群和胆汁酸代谢在多囊卵巢综合征发病机制中的作用[J].中山大学学报(医学科学版),2025,46(05):775-783.
LIN Kangyi,YIN Guoshu.Gut Microbiota and Bile Acid Metabolism in the Pathogenesis of Polycystic Ovary Syndrome[J].Journal of Sun Yat-sen University(Medical Sciences),2025,46(05):775-783.
林康毅,鄞国书.肠道菌群和胆汁酸代谢在多囊卵巢综合征发病机制中的作用[J].中山大学学报(医学科学版),2025,46(05):775-783. DOI: 10.13471/j.cnki.j.sun.yat-sen.univ(med.sci).2025.0507.
LIN Kangyi,YIN Guoshu.Gut Microbiota and Bile Acid Metabolism in the Pathogenesis of Polycystic Ovary Syndrome[J].Journal of Sun Yat-sen University(Medical Sciences),2025,46(05):775-783. DOI: 10.13471/j.cnki.j.sun.yat-sen.univ(med.sci).2025.0507.
多囊卵巢综合征(PCOS)是育龄期女性最常见的内分泌疾病之一,以排卵功能障碍、高雄激素血症及卵巢多囊样改变为核心特征,是导致女性不孕的主要原因,全球患病率达6%~20%。由于PCOS的复杂性和异质性,其发病机制目前尚未完全阐明,现有证据证明肠道菌群失调和胆汁酸代谢异常可能参与PCOS的发病过程。PCOS患者肠道菌群a多样性下降,产丁酸盐菌减少和拟杆菌属等有害菌增殖,导致肠道屏障受损和慢性炎症,并通过短链脂肪酸与性激素代谢失调加剧胰岛素抵抗和高雄激素血症。PCOS患者胆汁酸代谢异常表现为总胆汁酸水平升高、经典合成途径受损、替代途径激活和初级非结合胆汁酸异常累积。肠道菌群可影响胆汁酸的合成和代谢,胆汁酸也可调控肠道菌群的种类和丰度。肠道菌群-胆汁酸轴的双向调控异常促进PCOS的发生发展。因此,优化肠道菌群组成及调节胆汁酸代谢可能作为PCOS治疗的新靶点。相关机制的探索需结合动物模型和人群队列研究,解决个体化差异及安全性问题。本文对肠道菌群和胆汁酸代谢及其相互作用在PCOS发病机制的作用进行综述,并探讨其在治疗中的潜力,以期为理论研究和临床诊治提供参考。
Polycystic ovary syndrome (PCOS), one of the most prevalent endocrine disorders among women of reproductive age, is characterized by ovulatory dysfunction, hyperandrogenemia, and polycystic ovarian morphology. As a leading cause of female infertility, PCOS affects 6%-20% of women globally. The complex and heterogeneous nature of PCOS has hindered the full elucidation of its pathogenesis. Emerging evidence suggests that gut microbiota dysbiosis and abnormal bile acid metabolism may contribute to the development of PCOS. Patients with PCOS exhibit reduced a
lpha diversity of gut microbiota, marked by decreased butyrate-producing bacteria and the proliferation of harmful genera such as
Bacteroides
. This shift leads to intestinal barrier dysfunction, chronic inflammation, and exacerbation of insulin resistance and hyperandrogenemia through dysregulation of short-chain fatty acid and sex hormone metabolism. Additionally, PCOS patients display distinct bile acid metabolic abnormalities, including elevated total bile acids, impaired classical synthesis pathways, activated alternative pathways, and abnormal accumulation of primary unconjugated bile acids. A bidirectional regulatory axis exists between gut microbiota and bile acids: microbiota modulate bile acid synthesis and metabolism, while bile acids shape microbial composition and abundance. Dysregulation of this gut microbiota-bile acid axis promotes the pathogenesis of PCOS. Therefore, optimizing gut microbiota composition and modulating bile acid metabolism represent novel therapeutic targets for PCOS. Further mechanistic exploration requires integrated animal models and population-based cohort studies to address individualized variability and safety concerns. This review summarizes the roles of gut microbiota and bile acid metabolism in PCOS pathogenesis, highlights their interactions, and discusses therapeutic potential, aiming to provide insights for both theoretical research and clinical management.
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