Fetal androgen excess provides a developmental origin for polycystic ovary syndrome

摘要

Our 14-year study of a nonhuman primate model for polycystic ovary syndrome (PCOS) has provided substantial, experimentally derived evidence for fetal origins of PCOS that leads to lifelong reproductive and metabolic consequences [1-4]. Fetal androgen excess programming of PCOS-like pathophysiology is well established across the mammalian order, including rodents (mice and rats [5,6]), ungulates (sheep [7]) and higher primates (rhesus monkeys [8]), with such prenatally andro-genized females displaying an increased prevalence of at least two diagnostic criteria for PCOS in women.