Related Experiment Video
Updated: Mar 26, 2026

A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome
Published on: October 2, 2018
Androgens in polycystic ovary syndrome: lessons from experimental models
1Andrology Laboratory, ANZAC Research Institute, University of Sydney, Sydney, Australia.
Purpose Of Review:
There is substantial evidence to support a role for androgens acting via the androgen receptor in the development of the pathological disorder, polycystic ovary syndrome (PCOS). PCOS is the most common endocrine condition in women, but its etiology remains unknown. This review focuses on how animal experimental models of PCOS are providing strong evidence to support hyperandrogenism as an important mediator in the development of PCOS characteristics.
Recent Findings:
A variety of animal models for PCOS have now been established by increasing androgen exposure, supporting a role for androgens in the pathogenesis of PCOS. However, some androgens can be aromatized into estrogens leading to confusion on which PCOS traits are primary mediated via androgenic (mediated via the androgen receptor) or estrogenic (mediated via the estrogen receptor) mechanisms. Recent findings from studies comparing the induction of PCOS by aromatizable and nonaromatizable androgens, as well as androgen receptor knockout mouse models have enhanced our understanding of the mechanisms underlying PCOS, and verify that androgen receptor-mediated actions play a key role in the development of PCOS.
Summary:
Animal models have provided strong evidence to support that androgen receptor-mediated actions are key mediators in the development of PCOS traits.
Related Concept Videos
Oogenesis
Hormonal Control of the Ovarian Cycle
Before puberty, the hypothalamus releases GnRH in a low frequency, low amplitude pulsatile manner. This along with the immature hypothalamic-pituitary-gonadal axis activity, results in low estrogen levels and the absence of a fully functional ovarian cycle. At puberty, GnRH secretion increases in both frequency and...

