Semin Reprod Med 2011; 29(3): 173-186
DOI: 10.1055/s-0031-1275519
© Thieme Medical Publishers

Developmental Origin of Reproductive and Metabolic Dysfunctions: Androgenic Versus Estrogenic Reprogramming

Vasantha Padmanabhan1 , Almudena Veiga-Lopez2
  • 1Department of Pediatrics, Obstetrics and Gynecology, and Molecular and Integrative Physiology, The University of Michigan, Ann Arbor, Michigan
  • 2Department of Research Investigator, Department of Pediatrics, The University of Michigan, Ann Arbor, Michigan
Further Information

Publication History

Publication Date:
27 June 2011 (online)

ABSTRACT

Polycystic ovary syndrome (PCOS) is one of the most common fertility disorders, affecting several million women worldwide. Women with PCOS manifest neuroendocrine, ovarian, and metabolic defects. A large number of animal models have evolved to understand the etiology of PCOS. These models provide support for the contributing role of excess steroids during development in programming the PCOS phenotype. However, considerable phenotypic variability is evident across animal models, depending on the quality of the steroid administered and the perinatal time of treatment relative to the developmental trajectory of the fetus/offspring. This review focuses on the reproductive and metabolic phenotypes of the various PCOS animal models that have evolved in the last decade to delineate the relative roles of androgens and estrogens in relation to the timing of exposure in programming the various dysfunctions that are part and parcel of the PCOS phenotype. Furthermore, the review addresses the contributory role of the postnatal metabolic environment in exaggerating the severity of the phenotype, the translational relevance of the various animal models to PCOS, and areas for future research.

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Vasantha PadmanabhanPh.D. 

Professor, 300 North Ingalls, Room 1138, The University of Michigan

Ann Arbor, MI

Email: vasantha@umich.edu

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