Dong Xiao-Chao, Liu Chang, Zhuo Guang-Chao, Ding Yu
Department of Gynecology and Obstetrics, Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, People's Republic of China.
Central Laboratory, Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, People's Republic of China.
Diabetes Metab Syndr Obes. 2023 Jan 25;16:139-149. doi: 10.2147/DMSO.S393960. eCollection 2023.
Polycystic ovary syndrome (PCOS) is the most common heterogeneous endocrine disease that affecting females in reproductive age. Insulin resistance (IR), an important molecular basis for PCOS, accounts for at least 75% of women carrying this syndrome. Although there have been many studies on PCOS-IR, the detailed mechanisms are not fully understood. As essential hub for energy generation, mitochondria are critical to insulin secretion and normal function, whereas mutations in mitochondrial DNA (mtDNA) result in mitochondrial dysfunctions contributing to the pathophysiology of PCOS-IR via the regulation of balance of oxidative stress (OS), energy deficiency, or hormone metabolism. In the current review, we summarize the clinical and molecular features of PCOS-IR and discuss molecular mechanisms related to mtDNA mutations.
多囊卵巢综合征（PCOS）是影响育龄女性的最常见的异质性内分泌疾病。胰岛素抵抗（IR）是PCOS的重要分子基础，至少75%的该综合征女性患者存在胰岛素抵抗。尽管对PCOS-IR已有许多研究，但其详细机制尚未完全阐明。线粒体作为能量产生的关键枢纽，对胰岛素分泌和正常功能至关重要，而线粒体DNA（mtDNA）突变会导致线粒体功能障碍，通过调节氧化应激（OS）平衡、能量缺乏或激素代谢，参与PCOS-IR的病理生理过程。在本综述中，我们总结了PCOS-IR的临床和分子特征，并讨论了与mtDNA突变相关的分子机制。
