David H Abbott (1), Vasantha Padmanabhan (2) and Daniel A Dumesic (1,3 )
(1) National Primate Research Center, Department of Ob/Gyn, and Endocrinology-Reproductive Physiology Training Program, University of Wisconsin, Madison, WI 53715, USA
(2) Departments of Pediatrics, Ob/Gyn, Cellular and Integrative Physiology, and Reproductive Sciences Program, University of Michigan, Ann Arbor, MI 48109, USA
(3) Reproductive Medicine & Infertility Associates, Woodbury, MN 55125, USA
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.
Source: Reproductive Biology and Endocrinology 2006, 4:17.
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