Ontogeny of the ovary in polycystic ovary syndrome
Ovarian hyperandrogenism, hyperinsulinemia from insulin resistance, and altered intrafollicular paracrine signaling influence ovarian morphology, follicle survival, and growth as well as oocyte development in women with polycystic ovary syndrome.
Daniel A. Dumesic, M.D., JoAnne S. Richards, Ph.D.
Volume 100, Issue 1, Pages 23-38, July 2013
Activation of primordial follicles into the growing pool, selection of the dominant follicle and its eventual ovulation require complex endocrine and metabolic interactions, as well as intraovarian paracrine signals to coordinate granulosa cell proliferation, theca cell differentiation and oocyte maturation. Early preantral follicle development relies mostly upon mesenchymal-epithelial cell interactions, intraovarian paracrine signals and oocyte-secreted factors, while development of the antral follicle depends upon circulating gonadotropins as well as locally-derived regulators. In women with polycystic ovary syndrome (PCOS), ovarian hyperandrogenism, hyperinsulinemia from insulin resistance and altered intrafollicular paracrine signaling perturb activation, survival, growth and selection of follicles, causing accumulation of small antral follicles within the periphery of the ovary, giving it a polycystic morphology. Altered adipocyte-ovarian interactions further compound these adverse events on follicle development and also can harm the oocyte, particularly in the presence of increased adiposity. Finally endocrine antecedents of PCOS occur in female infants born to PCOS mothers and suggest that interactions between genes and the maternal-fetal hormonal environment may program ovarian function after birth.