Date of Award

5-2015

Degree Name

Master of Science

Department

Biological Sciences

First Advisor

Dr. Christopher A. Pearl

Second Advisor

Dr. Cindy Linn

Third Advisor

Dr. Pamela Hoppe

Keywords

Obesity, leptin receptor, hormones, spermato senesis. fertility

Access Setting

Masters Thesis-Abstract Only

Restricted to Campus until

5-15-2025

Abstract

The incidence of obesity and metabolic syndrome among the human population is increasing, but the effects on male fertility are unresolved. Leptin insensitivity appears to show a consistent relationship between obesity and fertility problems in men. Genetically modified mice lacking the leptin hormone (ob/ob) or leptin receptor (db/db) are reported to be subfertile and/or infertile but there is only minimal information about testicular function (sperm and hormone production) and the progression of infertility. Therefore, this study was designed to investigate testicular function using a leptin-receptor-deficient obese mouse model (the POUND mouse; Charles River). Testicular sperm production is reduced in POUND mice at 16 weeks of age leading to extremely low numbers of sperm in the epididymis. Thus, subfertility/infertility in these animals can be attributed, at least in part, to low sperm counts. However, sperm production is similar between POUND and c57 mice at 8 weeks suggesting that fertility problems in these leptin-receptor-deficient obese mice is the result of a progressive loss of testicular function after initiation of spermatogenesis.

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