Abstract
Polycystic ovary syndrome (PCOS) affects up to 10% of women worldwide, has a strong hereditary pattern with a heterogeneous phenotype. While no candidate genes have been found, a shared disease predisposing environment, such as intrauterine hyperandrogenemia, may explain an epigenetic inheritance pattern. A lean PCOS mouse model, eliminating the obesity confounder, with maternal androgen administration prenatally, provides an opportunity to study the effect of androgens on fetal programming.
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