Gut microbiota: an emerging target connecting polycystic ovarian syndrome and insulin resistance.

IF 4.8 2区 医学 Q2 IMMUNOLOGY Frontiers in Cellular and Infection Microbiology Pub Date : 2025-03-11 eCollection Date: 2025-01-01 DOI:10.3389/fcimb.2025.1508893
Yufeng Mei, Wanzhen Li, Bingqi Wang, Zhenni Chen, Xinyi Wu, Yingrui Lin, Min Wang
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Abstract

Polycystic ovary syndrome (PCOS) is a highly heterogeneous metabolic disorder, with oligomenorrhea and hirsutism as patients' primary complaints. Hyperinsulinemia is a crucial pathophysiological mechanism in the development of PCOS, with 50-70% of patients exhibiting insulin resistance (IR). This condition not only exacerbates ovulatory dysfunction but also leads to various adverse metabolic outcomes, such as dyslipidemia and diabetes, and increases the risk of cardiovascular events both before and after menopause. Gut microbiota is a microbial community within the host that possesses significant metabolic potential and is shaped by external environmental factors, the neuro-immune network, and metabolism. Recent studies have shown that gut microbiota dysbiosis is closely related to the development and progression of PCOS. Despite the growing recognition of the potential role of gut microbiota in the pathogenesis and treatment of PCOS, its clinical application remains in its infancy. Currently, most clinical guidelines and expert consensus still emphasize traditional therapeutic approaches, such as hormonal treatments, lifestyle modifications, and insulin sensitizers. However, accumulating evidence suggests that gut microbiota may influence the metabolic and reproductive health of PCOS patients through various mechanisms. Therefore, understanding the role of gut microbiota between PCOS and IR is essential. This review describes the changes in the gut microbiota of IR-PCOS patients, examines the potential mechanisms by which the gut microbiota contributes to IR in PCOS patients, and updates the evidence supporting the gut microbiota as a potential metabolic regulatory target in IR-PCOS. In summary, gut microbiota dysbiosis may be involved in the development and progression of IR in PCOS patients, and improving gut microbiota may offer metabolic stability benefits.

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肠道微生物群:连接多囊卵巢综合征和胰岛素抵抗的新靶点。
多囊卵巢综合征(PCOS)是一种高度异质性代谢紊乱,以少经和多毛为主要主诉。高胰岛素血症是多囊卵巢综合征发展的重要病理生理机制,50-70%的患者表现为胰岛素抵抗(IR)。这种情况不仅会加剧排卵功能障碍,还会导致各种不良代谢结果,如血脂异常和糖尿病,并增加绝经前后心血管事件的风险。肠道菌群是宿主体内具有重要代谢潜力的微生物群落,受外部环境因素、神经免疫网络和代谢的影响。近年来的研究表明,肠道菌群失调与多囊卵巢综合征的发生发展密切相关。尽管人们越来越认识到肠道微生物群在多囊卵巢综合征发病和治疗中的潜在作用,但其临床应用仍处于起步阶段。目前,大多数临床指南和专家共识仍然强调传统的治疗方法,如激素治疗、生活方式改变和胰岛素增敏剂。然而,越来越多的证据表明,肠道微生物群可能通过多种机制影响PCOS患者的代谢和生殖健康。因此,了解肠道菌群在PCOS和IR之间的作用是必要的。本文介绍了IR-PCOS患者肠道菌群的变化,探讨了肠道菌群参与PCOS患者IR的潜在机制,并更新了肠道菌群作为IR-PCOS潜在代谢调节靶点的证据。综上所述,肠道菌群失调可能参与了PCOS患者IR的发生和发展,改善肠道菌群可能提供代谢稳定的益处。
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来源期刊
CiteScore
7.90
自引率
7.00%
发文量
1817
审稿时长
14 weeks
期刊介绍: Frontiers in Cellular and Infection Microbiology is a leading specialty journal, publishing rigorously peer-reviewed research across all pathogenic microorganisms and their interaction with their hosts. Chief Editor Yousef Abu Kwaik, University of Louisville is supported by an outstanding Editorial Board of international experts. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide. Frontiers in Cellular and Infection Microbiology includes research on bacteria, fungi, parasites, viruses, endosymbionts, prions and all microbial pathogens as well as the microbiota and its effect on health and disease in various hosts. The research approaches include molecular microbiology, cellular microbiology, gene regulation, proteomics, signal transduction, pathogenic evolution, genomics, structural biology, and virulence factors as well as model hosts. Areas of research to counteract infectious agents by the host include the host innate and adaptive immune responses as well as metabolic restrictions to various pathogenic microorganisms, vaccine design and development against various pathogenic microorganisms, and the mechanisms of antibiotic resistance and its countermeasures.
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