Effects of Prenatal Testosterone Exposure on Female Reproduction: Alterations in Ovarian Function
Document Type
Oral Presentation
Campus where you would like to present
Ellensburg
Event Website
https://digitalcommons.cwu.edu/source
Start Date
15-5-2019
End Date
15-5-2019
Abstract
Polycystic ovarian syndrome (PCOS) is an endocrine disorder affecting 7-10% of women. PCOS causes reproductive and metabolic abnormalities such as multicystic ovaries, hyperandrogenism (excess testosterone), irregular menstrual cycles, obesity, and infertility. A PCOS mouse model can be created by injecting dihydrotestosterone (DHT) into mice to produce high levels of androgens that mimic symptoms seen in women with PCOS. Mice treated postnatally with DHT for 90 days have previously shown increased Claudin (Cldn) 3 and 11 gene expression in the ovary. In this study, mice were treated prenatally with DHT to examine the effects of excess testosterone on ovarian function and compare to a previously established postnatal model. Mice were also treated with flutamide, an androgen receptor inhibitor, to determine the mechanism through which testosterone affects ovarian function. We examined age of vaginal opening, anal genital distance, estrous cycle, and body weight as measurements of ovarian and metabolic phenotypes. At 8 weeks, mouse ovaries were used for quantitative Reverse Transcriptase PCR to examine the expression of Cldn 3 and 11 genes. Ovarian morphology was also observed. Prenatal DHT treatment did not affect Cldn 3 and 11 gene expression. Prenatal DHT treatment did not affect body weight consistently, however it did demonstrate reproductive abnormalities in vaginal opening, anal genital distance, and estrous cycle. The effects of DHT on ovarian function varied in the prenatal model compared to the postnatal model, which can provide a different model for determining the etiology of PCOS.
Recommended Citation
Gutierrez, Silvia and Magana, Jennifer, "Effects of Prenatal Testosterone Exposure on Female Reproduction: Alterations in Ovarian Function" (2019). Symposium Of University Research and Creative Expression (SOURCE). 46.
https://digitalcommons.cwu.edu/source/2019/Oralpres/46
Department/Program
Biological Sciences
Slides for SOURCE 2019 presentation Gutierrez
Additional Files
Silvia Gutierrez_SOURCE2019.pptx (6944 kB)Slides for SOURCE 2019 presentation Gutierrez
Effects of Prenatal Testosterone Exposure on Female Reproduction: Alterations in Ovarian Function
Ellensburg
Polycystic ovarian syndrome (PCOS) is an endocrine disorder affecting 7-10% of women. PCOS causes reproductive and metabolic abnormalities such as multicystic ovaries, hyperandrogenism (excess testosterone), irregular menstrual cycles, obesity, and infertility. A PCOS mouse model can be created by injecting dihydrotestosterone (DHT) into mice to produce high levels of androgens that mimic symptoms seen in women with PCOS. Mice treated postnatally with DHT for 90 days have previously shown increased Claudin (Cldn) 3 and 11 gene expression in the ovary. In this study, mice were treated prenatally with DHT to examine the effects of excess testosterone on ovarian function and compare to a previously established postnatal model. Mice were also treated with flutamide, an androgen receptor inhibitor, to determine the mechanism through which testosterone affects ovarian function. We examined age of vaginal opening, anal genital distance, estrous cycle, and body weight as measurements of ovarian and metabolic phenotypes. At 8 weeks, mouse ovaries were used for quantitative Reverse Transcriptase PCR to examine the expression of Cldn 3 and 11 genes. Ovarian morphology was also observed. Prenatal DHT treatment did not affect Cldn 3 and 11 gene expression. Prenatal DHT treatment did not affect body weight consistently, however it did demonstrate reproductive abnormalities in vaginal opening, anal genital distance, and estrous cycle. The effects of DHT on ovarian function varied in the prenatal model compared to the postnatal model, which can provide a different model for determining the etiology of PCOS.
https://digitalcommons.cwu.edu/source/2019/Oralpres/46
Faculty Mentor(s)
April Binder