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Review
. 2019 Jun 3;20(11):2720.
doi: 10.3390/ijms20112720.

Animal Models for Human Polycystic Ovary Syndrome (PCOS) Focused on the Use of Indirect Hormonal Perturbations: A Review of the Literature

Youngjae Ryu  1 , Sung Woo Kim  2 , Yoon Young Kim  3   4 , Seung-Yup Ku  5   6
Affiliations
Review

Animal Models for Human Polycystic Ovary Syndrome (PCOS) Focused on the Use of Indirect Hormonal Perturbations: A Review of the Literature

Youngjae Ryu et al. Int J Mol Sci. .

Abstract

Hormonal disturbances, such as hyperandrogenism, are considered important for developing polycystic ovary syndrome (PCOS) in humans. Accordingly, directly hormone-regulated animal models are widely used for studying PCOS, as they replicate several key PCOS features. However, the pathogenesis and treatment of PCOS are still unclear. In this review, we aimed to investigate animal PCOS models and PCOS-like phenotypes in animal experiments without direct hormonal interventions and determine the underlying mechanisms for a better understanding of PCOS. We summarized animal PCOS models that used indirect hormonal interventions and suggested or discussed pathogenesis of PCOS-like features in animals and PCOS-like phenotypes generated in other animals. We presented integrated physiological insights and shared cellular pathways underlying the pathogenesis of PCOS in reviewed animal models. Our review indicates that the hormonal and metabolic changes could be due to molecular dysregulations, such as upregulated PI3K-Akt and extracellular signal-regulated kinase (ERK) signalling, that potentially cause PCOS-like phenotypes in the animal models. This review will be helpful for considering alternative animal PCOS models to determine the cellular/molecular mechanisms underlying PCOS symptoms. The efforts to determine the specific cellular mechanisms of PCOS will contribute to novel treatments and control methods for this complex syndrome.

Keywords: animal models; ovary; pathogenesis; polycystic ovary syndrome.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
A schematic representation of the summarized pathophysiology to explain the manifestation of elevated testosterone levels and polycystic ovary (PCO) morphology. Solid lines indicate direct effects, and dotted lines, relatively weak or indirect effects. Two-headed arrows present cross-actions.
Figure 2
Figure 2
Suggested and integrated molecular signalling possibly related to PCOS development. Solid lines indicate direct effects, and dotted lines, indirect effects. PIP2 = phosphatidylinositol-4,5-bisphosphate, PIP3 = phosphatidylinositol-3,4,5-trisphosphate.
See this image and copyright information in PMC

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