Читать книгу Hyperandrogenism in Women - Группа авторов - Страница 19

Mounting evidence from human and animal studies repeatedly implicates appropriately timed in utero androgen excess, from either maternal and/or fetal sources, as high risk for PCOS emerging at adolescence. Figure 1 provides a diagrammatic representation of maternal and fetal sources of gestational androgen excess, taken together with relevant PCOS risk genes, may programme for ovarian androgen excess. Figure 2 illustrates hypothetical sites for female reprogramming mediated by androgen receptor, as identified by genetically manipulated mouse studies [17, 18]. Such a unified hypothetical model is compatible with postnatal androgen-activated reprogrammed functions, such that anti-androgens or androgen-diminishing consequences of weight loss interventions, including lifestyle, diet, bariatric surgery, and insulin-sensitizing treatments, ameliorate PCOS traits in adulthood. Increasing sophistication of bioinformatics to assess risk for functional outcome of genomic and epigenomic variants vulnerable to in utero androgen excess, hold promise for identification of PCOS risk in newborn, enabling early intervention.