Journal
REPRODUCTIVE BIOLOGY AND ENDOCRINOLOGY
Volume 4, Issue -, Pages -Publisher
BMC
DOI: 10.1186/1477-7827-4-17
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Funding
- NCRR NIH HHS [C06 RR015459, C06 RR020141, RR020141-01, P51 RR000167, R21 RR014093, RR15459-01, R01 RR013635] Funding Source: Medline
- NIA NIH HHS [T32 AG000268] Funding Source: Medline
- NICHD NIH HHS [P01 HD044232, R01 HD041098, P50 HD044405, U01 HD044650] Funding Source: Medline
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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.
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