Endocrine Abstracts

JOINT3116

Polycystic ovary syndrome (PCOS) is an endocrine disorder characterized by exacerbated ovarian androgen production. When PCOS is accompanied by obesity and insulin resistance, reproductive dysfunction is usually even more pronounced. Granulosa cells (GCs) play a pivotal role in oocyte maturation, as key regulators of ovarian steroidogenesis and physiology. Consequently, GCs metabolic dysfunction can disrupt follicular development and potentially result in anovulation. However, the extent to which GC metabolic function is affected in the presence of PCOS remains largely unknown. This study aim was to explore whether the follicular fluid (FF) microenvironment is able to influence GC glycolytic function. The study enrolled 24 women undergoing controlled ovarian stimulation for infertility treatment: 12 with PCOS and 12 controls. Each group was further subdivided according to BMI, normal weight (n = 6; BMI < 25 kg/m²) and obesity (n = 6; BMI ≥ 30 kg/m²). Human granulosa cells (HGrC1) were incubated for 24 hours in culture medium supplemented with 20% of FF collected during oocyte retrieval from women with PCOS or controls. Glycolytic function was assessed by measuring the extracellular acidification rate (ECAR). HGrC1 cells when exposed to FF from women with PCOS and obesity depicted a significantly lower glycolytic capacity when compared to those incubated with FF from normal-weight controls. Furthermore, non-glycolytic acidification of HGrC1 cells incubated with FF from women with PCOS irrespective of BMI was significantly lower than of those incubated with FF from normal-weight controls. These findings indicate that the FF from women with PCOS and obesity harbours the potential to impair granulosa cell glycolytic function, while suggesting that GC metabolic disruptions could underlie ovarian dysfunction in women with PCOS, particularly when associated with obesity.