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• W2597127974 abstract "Testosterone (T) treatment of fetal lambs from 30–90 d of gestation (T60; term 147 d) leads to hypergonadotropism, multifollicular ovaries and follicular persistence. The disrupted ovarian follicular dynamics may be the consequence of neuroendocrine defects resulting in altered gonadotropic drive or, alternatively, compromised ovarian sensitivity to gonadotropins. To test the hypothesis that reproductive dysfunction in T60 ewes is a consequence of abnormal gonadotropic drive, release of endogenous LH and biopotent FSH was blocked by administering gonadotropin-releasing hormone antagonist (GnRHA; acyline; 10 μg/Kg, 12-hourly) to control (C, n = 5) and T60 (n = 5) ewes for 9 days. On day 7 of GnRHA treatment, ewes were injected with LH (0.108 μg/kg) and native ovine FSH (0.173 μg/kg) at 2-h intervals for 36 h followed by hourly injections of LH (0.054 μg/kg) and a combination (1:4 ratio) of native FSH (0.043 μg/kg) and asialo FSH (FSH exposed to neuroaminidase; 0.173 μg/kg) for the next 12 h. Native FSH is less biopotent with a longer half life. Asialo FSH is short-lived but more biopotent. All ewes were then given 1500 IU of hCG to induce ovulation. Plasma estradiol (E) was measured at 4-h intervals during the LH/FSH drive. Transrectal ultrasonography was performed to monitor ovarian follicular dynamics at the start of GnRHA and daily beginning 1 d before and concluding 4 d after LH/FSH administration. Ultrasonography also was performed 10 d after hCG to assess corpus luteum (CL) development. Follicle number and diameter, basal and peak E concentrations and temporal changes in follicular size classes were analyzed by ANOVA, with repeated measures as needed. Total number of follicles tended to be greater (P=0.09) in T60 ewes before the start of GnRHA treatment. Six days after exposure to GnRHA, T60 ewes continued to have a greater number of follicles (P<0.05) due to increased number of <2 mm follicles (P<0.01). With advancing LH/FSH treatment, a progressive increase (P<0.01) in >4–8 mm size follicles (ovulatory range) were evident in both groups and there were no treatment differences. After hCG, follicles from both C and T60 females continued to grow (P<0.01) with some achieving >12–20 mm in size. The number of CL (C:4.0 ± 1.5; T60:3.8 ± 0.5) and luteal cysts (C:5.0 ± 1.1; T60:6.0 ± 3.3) did not differ between C and T60. Concentrations of E (pg/mL) were similar (C:9.1 ± 1.6; T60: 10.8 ± 1.1) at the start of FSH treatment. Peak circulating E (C:4.5 ± 1.1; T60: 7.1 ± 1.8) and area under the E curve (C:17.6 ± 3.4; T60: 31.8 ± 7.8) were similar after LH/FSH treatment. Based on these findings, we suggest that exogenous gonadotropin treatment following blockade of GnRH action with GnRHA equalized the follicular and circulating E responses of T60 to that of C. The superstimulation achieved with more biopotent, short-lived asialo FSH did not allow proper testing of the hypothesis. Development of follicles >12–20 mm that persisted even after hCG in both C and T60 females indicated that these follicles may have persisted because they failed to develop the attributes of a preovulatory follicle, perhaps due to the asialo FSH provided. Abnormal FSH drive may, therefore, be one mechanism by which follicular persistence may have occurred in prenatal T females. This study emphasizes the need for proper ovarian stimulation protocols to reduce the risk for multiple pregnancy and ovarian hyperstimulation syndrome. Supported by NIH-HD 41098 & P01 HD 4423. (platform)" @default.
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• W2597127974 date "2007-07-01" @default.
• W2597127974 modified "2023-09-26" @default.
• W2597127974 title "DEVELOPMENTAL PROGRAMMING: DO EXOGENOUS GONADOTROPINS NORMALIZE OVARIAN FUNCTION IN PRENATAL TESTOSTERONE-TREATED FEMALES?" @default.
• W2597127974 doi "https://doi.org/10.1093/biolreprod/77.s1.212" @default.
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