Högskolan i Skövde

Polycystic ovary syndrome is a common endocrine disorder that hinders women’s metabolism and reproductive health characterized by elevated androgen levels, polycystic ovaries, infertility, hirsutism, inflammation, obesity and insulin resistance. Research suggests mitochondrial dysfunction as an underlying cause of PCOS. This study aimed to develop a PCOS model of Drosophila melanogaster by induction of androgens (testosterone). The eggs of the wild-type stock flies were exposed to ethanol (control) and varying doses of testosterone (1-10mg/kg) and examined throughout development. Androgen and ethanol exposure caused alterations in the external morphology and ovarian appearance suggesting a link to PCOS-related symptoms. Fertility measured by fecundity rates decreased by 32.6% in androgen treated flies, though statistical tests revealed no significant differences between groups. Androgen exposure altered the mitochondrial gene expression but with no statistical difference between conditions in all genes (p values: MTCO1 = 0.368; SOD1 = 0.276; ATPsynthase = 0.102). MTCO1 showed approximately a 99% difference in low and high testosterone groups from control. SOD1 increased by 7645.72% and 98.8%, and ATPsynthase by 319.9% and 703.4%in low and high testosterone conditions, respectively. Triglyceride levels were elevated in androgen groups across F1 and F2 generations, indicating potential metabolic disruptions. Significant differences revealed between control and high testosterone (F1, p = 0.04; F2, p = 0.006) but not in low testosterone (F1, p = 0.402; F2, p = 0.328). Lack of significant findings renders the results unreliable. Future research with broader gene panels and improved methologies are required to validate the model's applicability for PCOS research.