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Defects in Hormone Cycling After Prenatal Testosterone

Obesity exacerbates defects in sheep; may explain aspects of polycystic ovary syndrome

THURSDAY, Mar. 5 (HealthDay News) -- Female sheep that were exposed to excess testosterone in utero have defects in reproductive hormone cycling, particularly if they become obese, researchers report in the March issue of Endocrinology. The observations may explain the anovulation observed in obese women with polycystic ovary syndrome, where excess prenatal steroid exposure may play a role in the disease.

Teresa L. Steckler, from the University of Michigan in Ann Arbor, and colleagues injected pregnant sheep twice a week with testosterone during early to mid-gestation (30 to 90 days). A subset of female offspring of control or testosterone-treated sheep were overfed starting at 14 weeks after birth.

The researchers found that prenatal testosterone had no effect on the timing of puberty, but overfed female offspring of testosterone-treated mothers stopped cycling earlier. Definable surges of luteinizing hormone were observed in all controls, 71 percent of overfed controls, 43 percent of prenatal testosterone sheep and only 14 percent of overfed prenatal testosterone sheep. Only 14 percent of overfed prenatal testosterone-treated females had a luteal progesterone increase compared with nearly all animals in the other groups. Both overfeeding and prenatal testosterone independently increased the pulse frequency of luteinizing hormone during the anestrous season, the authors report.

"These findings agree with the increased prevalence of anovulation observed in obese women with polycystic ovary syndrome and indicate that excess postnatal weight gain amplifies reproductive disruptions caused by prenatal testosterone excess," Steckler and colleagues conclude.

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