In female mammals, including humans, deviations from normal androgenic or estrogenic exposure during fetal development are detrimental to subsequent adult ovarian function.
Androgen deficiency, without accompanying
estrogen deficit, has little apparent impact on ovarian development. Fetal
estrogen deficiency, on the other hand, results in impaired oocyte and follicle development, immature and abnormal adult ovaries, and excessive ovarian stimulation from endogenous
gonadotropins ultimately generating hemorrhagic follicles. Complete
estrogen deficiency lasting into adulthood results in partial ovarian masculinization. Fetal
androgen excess, on the other hand, mediated either by direct
androgen action or following
androgen aromatization to
estrogen, reprograms ovarian development and reproductive neuroendocrinology to mimic that found in women with
polycystic ovary syndrome: enlarged, polyfollicular, hyperandrogenic, anovulatory ovaries with accompanying LH hypersecretion. Oocyte developmental competence is also compromised.
Insulin is implicated in the mechanism of both
anovulation and deficient oocyte development. Fetal
estrogen excess induces somewhat similar disruption of adult ovarian function to fetal
androgen excess. Understanding the quality of the fetal female
sex steroid hormone environment is thus becoming increasingly important in improving our knowledge of mechanisms underlying a variety of female reproductive pathologies.