title: Effect of maternal PCOS and PCOS-like phenotype on the offspring's health.
abstract: Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine disorder with both reproductive and metabolic abnormalities affecting women of reproductive age. While the exact origin of PCOS is unknown, observations from clinical and animal studies suggest that maternal hyperandrogenism may be a contributing factor. Because women with PCOS manifest hyperandrogenism during pregnancy, changes in the gestational endocrine milieu may play a role in the vertical transmission of this syndrome. This review discusses the potential developmental origins of PCOS, the impact of maternal PCOS on the offspring's health and contributions of the postnatal environment, capitalizing on findings from animal models that exhibit a PCOS-like phenotype. In addition, this review highlights the scarcity of data at early gestational stages in humans and the importance of animal experimentation to better understand the cellular and molecular mechanisms involved in the programming of adult diseases, therefore, helping identify therapeutic targets for preventive and treatment strategies.
authors.affiliation: Department of Pediatrics, University of Michigan, Ann Arbor, MI 48109, USA.
authors.forename: Muraly
authors.initials: M
authors.lastname: Puttabyatappa
authors.affiliation: Department of Pediatrics, University of Michigan, Ann Arbor, MI 48109, USA.
authors.forename: Rodolfo C
authors.initials: RC
authors.lastname: Cardoso
authors.affiliation: Department of Pediatrics, University of Michigan, Ann Arbor, MI 48109, USA. Electronic address: vasantha@umich.edu.
authors.forename: Vasantha
authors.initials: V
authors.lastname: Padmanabhan
mesh_terms: D000328:Adult; D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D017588:Hyperandrogenism / Q000503:physiopathology*; D010641:Phenotype; D011085:Polycystic Ovary Syndrome / Q000150:complications*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000209:etiology*
keywords: Androgen; Animal models; Developmental programming; Insulin; Polycystic ovary syndrome