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Updated: Aug 19, 2025

A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome
Published on: October 2, 2018
Hyperandrogen-induced polyol pathway flux increase affects ovarian function in polycystic ovary syndrome via
Yi-Cheng Wang1, Yong-Dan Ma2, Huan Liu2
1Department of Physiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu 610041, Sichuan, China; Department of Reproductive Health and Infertility, Chengdu Women's and Children's Central Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu 611731, Sichuan, China.
Aims:
Polycystic ovary syndrome (PCOS) is a common endocrine disorder in the women of childbearing age. It is characterized by hyperandrogenism and abnormal follicular growth and ovulation. The polyol pathway is a glucose metabolism bypass pathway initiated by aldose reductase (ADR). Androgen induces the expression of ADR in the male reproductive tract, which has a general physiological significance for male reproductive function. Here we investigate whether hyperandrogenemia in PCOS leads to increased flux of the polyol pathway in ovarian tissue, which in turn affects follicular maturation and ovulation through oxidative stress.
Main Methods:
We used clinical epidemiological methods to collect serum and granulosa cells from clinical subjects for a clinical case-control study. At the same time, cell biology and molecular biology techniques were used to conduct animal and cell experiments to further explore the mechanism of hyperandrogen-induced ovarian polyol pathway hyperactivity and damage to ovarian function.
Key Findings:
Here, we find that hyperandrogenism of PCOS can induce the expression of ovarian aldose reductase, which leads to the increase of the polyol pathway flux, and affects ovarian function through excessive oxidative stress.
Significance:
Our research has enriched the pathological mechanism of PCOS and may provide a new clue for the clinical treatment of PCOS.
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