Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 548-560-Hyperandrogenic Disorders
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-552
Pedro Pablo Rojas-Garcia*1, Monica Patricia Recabarren1, Daniel Sandoval1, Albert Carrasco1, Romina Fornes1, Teresa Sir-Petermann2 and Sergio E Recabarren1
1University of Concepcion, Chillan, Chile, 2University of Chile, Santiago, Chile
The reprogramming effects of prenatal exposure to excess testosterone (T) on postnatal reproductive and metabolic parameters have been studied extensively in females, but similar studies during the fetal development are still scarce. We have previously found prenatal T treatment leads to offspring with reduced birth weight and masculinization of the genitalia, impaired insulin sensitivity, a tendency to an early onset of puberty, greater pituitary gland sensitivity to GnRH and high ovary sensitivity to endogenous LH stimulation during postnatal life. If such disruptions are established during fetal development, because of the changes of the fetal endocrine environment due to T treatment, remain to be explored. This study addressed the impact of prenatal T excess on ovarian morphology and expression of genes modulating ovarian function: Antimüllerian hormone (AMH), FSH receptor (FSHR), and androgen receptor (AR) in fetuses of 120 days. Pregnant Suffolk sheep were administered either testosterone propionate 30 mg (from day 30 to 90) followed by 40 mg (from day 90 to 120) i.m. twice weekly of pregnancy (term is ~147 days) or vehicle. At 120 days of pregnancy, dams were sedated and subsequently maintained under general anesthesia. The gravid uterus was exposed and the fetuses were removed for body measures and were given an intracardiac barbiturate prior to tissue harvest. Histological parameters were measured using light microscopy and mRNA expression was measured using real time PCR. Body and ovarian weight were similar between female fetuses of both groups of dams, ruling out the effect of weight on the presented results. The number of primordial, primary and secondary follicles was similar between T- and C-females fetuses which may reveal unaltered environment that promotes growing of those types of follicles, like AMH. In fact AMH expression was similar between groups and so was the expression of FSHR and AR in the ovarian tissue. However, T-females fetuses showed the presence of antral follicles, which were absent in C-females. These latter findings suggest that the effects of prenatal T on the ovary paracrine control of antrum development is not dependant on AMH, or FSH and androgen pathways, or that other factors not studied in this experiment may be involved in the triggering of antrum development

Nothing to Disclose: PPR, MPR, DS, AC, RF, TS, SER

*Please take note of The Endocrine Society's News Embargo Policy at

Sources of Research Support: Supported by Fondecyt Grant 1090031