Student: Nicholas Werner (School of Graduate Studies)
Mentor: April Binder
Polycystic ovary syndrome (PCOS) is the leading cause of infertility, and the most common endocrine disorder among women of reproductive age, affecting between 8-12% of the population worldwide. PCOS is characterized by cystic ovaries, hormonal irregularities, and metabolic dysfunction. The metabolic dysfunctions associated with PCOS may include obesity, glucose intolerance, and type II diabetes. Because hormonal irregularities are the primary cause of the metabolic symptoms, they are difficult to treat. However, previous studies conducted on the gene NAG-1 have shown it may prevent metabolic disorders when overexpressed. Studies on NAG-1 have focused on diet induced metabolic disorders, and not hormonally induced disorders like those seen in PCOS. Our study focuses on NAG-1, and if it can prevent any of the metabolic disorders associated with PCOS. To study this, we induced PCOS in mice via dihydrotestosterone (DHT) implant, and monitored them for 90 days, after which tissue and serum samples were collected for analysis. We observed no change in weight between the NAG-1 DHT and placebo groups, suggesting NAG-1 may prevent hormonal induced obesity. We also observed no changes in adipocyte sizes between the NAG-1 groups. DHT treated animals entered puberty at an earlier age than placebo groups and ovarian dysfunction was observed. DHT treated animals had disrupted estrus cycles and significantly less corpus lutea in their ovary, suggesting altered ovarian function. WT placebo and DHT groups had significant differences in all aforementioned metabolic phenotypes. Our findings suggest that overexpression of NAG-1 may prevent some metabolic dysfunctions associated with PCOS.