4.8 Article

The Goto-Kakizaki rat is a spontaneous prototypical rodent model of polycystic ovary syndrome

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NATURE COMMUNICATIONS
卷 12, 期 1, 页码 -

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NATURE PORTFOLIO
DOI: 10.1038/s41467-021-21308-y

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  1. l'Agence Nationale pour la Recherche [ANR-12-BSV1-0034-01]
  2. Inserm Transfert [MAT-PI-13357-B-01]
  3. Inserm
  4. Sorbonne University
  5. Medical Research Foundation (grant FRM) [EQU201903007868]
  6. Ministere de l'Enseignement Superieur et de la Recherche
  7. Agence Nationale de la Recherche (ANR) [ANR-12-BSV1-0034] Funding Source: Agence Nationale de la Recherche (ANR)

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The authors report a rat model that spontaneously exhibits the clinical heterogeneity of PCOS and demonstrate that the phenotype is developmentally programmed. This rodent model provides a novel tool for identifying the mechanisms involved in the pathogenesis of PCOS and developing new treatment strategies.
Polycystic ovary syndrome (PCOS) is characterized by an oligo-anovulation, hyperandrogenism and polycystic ovarian morphology combined with major metabolic disturbances. However, despite the high prevalence and the human and economic consequences of this syndrome, its etiology remains unknown. In this study, we show that female Goto-Kakizaki (GK) rats, a type 2 diabetes mellitus model, encapsulate naturally all the reproductive and metabolic hallmarks of lean women with PCOS at puberty and in adulthood. The analysis of their gestation and of their fetuses demonstrates that this PCOS-like phenotype is developmentally programmed. GK rats also develop features of ovarian hyperstimulation syndrome. Lastly, a comparison between GK rats and a cohort of women with PCOS reveals a similar reproductive signature. Thus, this spontaneous rodent model of PCOS represents an original tool for the identification of the mechanisms involved in its pathogenesis and for the development of novel strategies for its treatment. Although polycystic ovary syndrome is the most common cause of female infertility, its etiology remains poorly understood. Here, the authors report a rat model that spontaneously exhibits the clinical heterogeneity of this syndrome and demonstrate that the phenotype is developmentally programmed.

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