Reproduction Abstracts

Polycystic ovary syndrome (PCOS) is a common endocrinopathy that is associated with anovulatory infertility, menstrual disturbances as well as an adverse metabolic profile. Hyperandrogenism is the hallmark of PCOS and originates predominantly from ovarian theca cells. Obesity increases androgen synthesis, partly due to accompanying hyperinsulinemia but also as a result of an effect of adipokines on ovarian steroidogenesis (Comim et al. PLoS ONE 8, 2013). Adipokines are factors secreted by adipose tissue and while adipokines are known to increase androgen synthesis, the effect of hyperandrogenism on adipokines is less clear. In this study, we investigated the effect of excess androgens on adipocyte differentiation and adipokine gene expression. Immortalised multi-depot mouse preadipocytes were differentiated for 14 days in the presence and absence of dihydrotestosterone (DHT). In addition, fully differentiated adipocytes were treated with DHT or control for 24 h. Adipogenesis was observed using Oil Red O and quantitative PCR was used to analyse gene expression for a panel of 25 adipokines. Our results show that hyperandrogenism leads to dysregulation of adipokine gene expression. Several adipokines thought to be involved in modulating ovarian androgen secretion are significantly perturbed. These include downregulation of adiponectin (P<0.05) and upregulation of visfatin (P<0.05). Other changes include distinctive adipokine profiles similar to those found in metabolic syndrome such raised PAI1 (P<0.05) as well as a downregulation of adipokines related to energy expenditure and brown adipose tissue identity. These results support the existence of a reciprocal relationship between hyperandrogenism and adipokine secretion.