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Review
. 2019 Aug 28;7(9):89.
doi: 10.3390/medsci7090089.

The Mechanism of Androgen Actions in PCOS Etiology

Valentina Rodriguez Paris  1 , Michael J Bertoldo  2   3
Affiliations
Review

The Mechanism of Androgen Actions in PCOS Etiology

Valentina Rodriguez Paris et al. Med Sci (Basel). .

Abstract

Polycystic ovary syndrome (PCOS) is the most common endocrine condition in reproductive-age women. By comprising reproductive, endocrine, metabolic and psychological features-the cause of PCOS is still unknown. Consequently, there is no cure, and management is persistently suboptimal as it depends on the ad hoc management of symptoms only. Recently it has been revealed that androgens have an important role in regulating female fertility. Androgen actions are facilitated via the androgen receptor (AR) and transgenic Ar knockout mouse models have established that AR-mediated androgen actions have a part in regulating female fertility and ovarian function. Considerable evidence from human and animal studies currently reinforces the hypothesis that androgens in excess, working via the AR, play a key role in the origins of polycystic ovary syndrome (PCOS). Identifying and confirming the locations of AR-mediated actions and the molecular mechanisms involved in the development of PCOS is critical to provide the knowledge required for the future development of innovative, mechanism-based interventions for the treatment of PCOS. This review summarises fundamental scientific discoveries that have improved our knowledge of androgen actions in PCOS etiology and how this may form the future development of effective methods to reduce symptoms in patients with PCOS.

Keywords: PCOS; androgens; fertility.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
PCOS features and the reported effects of androgen blocking treatments in women with PCOS.
Figure 2
Figure 2
Proposed optimal period for exposure of excess androgens to induce the PCOS phenotype in animal models. Diagram of rodent, sheep and primate PCOS animal models and their prenatal or postnatal period of exposure to androgens to give rise to the PCOS phenotype observed in humans. T = Testosterone DHT = Dihydrotestosterone DHEA = Dehydroepiandrosterone.
Figure 3
Figure 3
The most recent understanding of androgen receptor mechanisms proposed to be involved in PCOS trait development. Here we illustrate the two proposed axes involved in the development of reproductive and metabolic features of PCOS resulting from androgen excess and the consequential PCOS traits developed.
See this image and copyright information in PMC

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