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.

Faculty Mentor(s)

April Binder

Department/Program

Biological Sciences

Silvia Gutierrez_SOURCE2019.pptx (6944 kB)
Slides for SOURCE 2019 presentation Gutierrez

Additional Files

Silvia Gutierrez_SOURCE2019.pptx (6944 kB)
Slides for SOURCE 2019 presentation Gutierrez

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May 15th, 12:00 AM May 15th, 12:00 AM

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