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Presentation date

Summer 8-10-2022

Faculty Mentor

Dr. John S. Davis

Research Mentor

Dr. Michele R. Plewes

Abstract

Infertility affects 1 out of every 6 couples, worldwide, with male infertility playing a primary factor in a third of all cases. Dysregulation of sex hormones is a major cause of infertility. Male hypogonadism is a condition in which the testis does not produce adequate concentrations of testosterone. Males suffering from hypogonadism can be born with the condition or develop it later in life, often from acute injury or infection. Male hypogonadism is treated with testosterone replacement to return testosterone levels to normal. However, one side effect of testosterone treatment is infertility. Understanding mechanisms that regulate the synthesis of sex steroids holds great potential to positively impact reproductive health and overall quality of life. Mitochondria play a key role in the synthesis of all steroid hormones. The first and rate-limiting step in the production of all steroid hormones is the transfer of cholesterol from the outer mitochondrial membrane to the inner membrane. In the current study, we examined the hypothesis that mitochondrial fusion promotes acute steroid synthesis in LH-responsive Leydig cells.

Keywords

Mitochondrial Fusion, Hypogonadism, Leydig cells, OPA, MFN, Leflunomide, MYLS22, Mitochondrial Fusion Promoter

Mitochondrial Fusion Promotes Steroidogenesis in MA10 Leydig Cells

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