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Submitted on November 4, 2004
Accepted on March 24, 2005
Department of Pediatrics and the Reproductive Sciences Program, University of Michigan, Ann Arbor, MI; Department of Obstetrics and Gynecology and Cellular and Integrative Physiology, University of Nebraska, Omaha, NE; Department of Animal Sciences, Cellular and Molecular Biosciences Program, Auburn University, AL
* To whom correspondence should be addressed. E-mail: vasantha{at}umich.edu.
Exposure to testosterone (T) during days 30 to 90 of fetal life results in low birth weight offspring, hypergonadotropism, multifollicular ovaries, and early cessation of cyclicity. The multifollicular phenotype may result from failure of follicles to regress and consequent follicular persistence or, alternatively, increased follicular recruitment. We tested the hypothesis that prenatal exposure to excess T causes intrauterine growth retardation (IUGR) and increases ovarian follicular recruitment. Time-mated pregnant ewes were treated with 100 mg T propionate in cottonseed oil or vehicle twice weekly from day 30 to 90 of gestation. Ewes were euthanized near term, between days 139 to 141 of gestation (term is 147 days). After determining fetal measures and organ weights, ovaries were removed from fetuses of control and T-treated dams and follicular distribution in each ovary was determined by morphometric quantification. Total number and percentage distribution of the various classes of follicles (primordial, primary, preantral, and antral follicles) were compared between treatment groups. Prenatally T-treated female fetuses were smaller in size, had an increased head circumference to fetal weight ratio (P<0.01), increased adrenal to fetal weight ratio (P<0.05), decreased number of follicles (P<0.05), a decrease in percentage of primordial follicles (P<0.001), and a corresponding increase in the remaining classes of follicles (P<0.05). Ovarian findings support decreased ovarian reserve and enhanced follicular recruitment, potential contributors of early reproductive failure. The extent to which metabolic changes associated with IUGR contribute toward altered trajectory of ovarian folliculogenesis remains to be determined.
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