ECEESPE2025 Poster Presentations Reproductive and Developmental Endocrinology (93 abstracts)
1UMIB - Unit for Multidisciplinary Research in Biomedicine, ICBAS - School of Medicine and Biomedical Sciences, University of Porto, 4050-313 Porto, Portugal, Porto, Portugal; 2ITR - Laboratory for Integrative and Translational Research in Population Health, 4050-600 Porto, Portugal, Porto, Portugal; 3Centre for Medically Assisted Procreation/Public Gamete Bank, Gynecology Department, Centro Materno-Infantil do Norte Dr. Albino Aroso (CMIN), Centro Hospitalar Universitário de Santo António (CHUdSA), Unidade Local de Saúde de Santo António (ULSSA), 4099-001 Porto, Portugal, Porto, Portugal; 4CEIE Centro de Estudos de Infertilidade e Esterilidade, 4050-345 Porto, Portugal, Porto, Portugal
JOINT3391
Polycystic ovary syndrome (PCOS) is an endocrine disorder characterized by oligo-ovulation, clinical or biochemical hyperandrogenemia and polycystic ovaries, which affect reproductive function. Besides anovulation, there are several other hormone and metabolic factors that can have a negative impact in fertility outcomes of women with PCOS. Conception requires ovulation of a mature oocyte and the presence of mature spermatozoa. During ovulation, the oocyte is released into the oviduct along with follicular fluid (FF) that modulates its fluid composition, while within the oviduct spermatozoa undergo capacitation that is required for fertilization. The FF hormone and metabolic profile of women with PCOS is known to depict distinctive molecular fingerprints. However, whether the FF profile associated with PCOS affects spermatozoa capacitation is unknown, which this study aimed to disclose. For this purpose, spermatozoa were isolated from seminal fluid of men with normozoospermia (n = 12) and incubated with FF collected from women undergoing in vitro fertilization (IVF) treatments. FF was harvested from age-matched women with PCOS and normal weight (BMI < 25kg/m2; PCOS; n = 6), women with PCOS and obesity (BMI > 30 kg/m2; PCOS+Ob; n = 6) and normo-ovulatory women with normal weight (BMI < 25kg/m2, CTRL; n = 6) submitted to IVF treatments due to tubal and/or male infertility factors. FF of each group was pooled before incubation with spermatozoa. Spermatozoa isolated from seminal fluid were incubated in capacitating medium (BWW) at 37ºC. After the first 2h of incubation, spermatozoa were treated with 20% pooled FF from each group (CTRL, PCOS, PCOS+Ob) for an additional 1h. Vitality and motility (total and progressive) were assessed hourly. While the FF did not affect vitality at all tested conditions, the progressive motility was significantly increased after incubation with FF from CTRL as compared to the pre-treatment conditions (48.76±12.74% vs 38.69±17.33%, P = 0.0251), which was not observed after incubation with FF from PCOS (36.57±16.81%, P = 0.8895) nor PCOS+Ob (35.69±16.17%, P = 0.6560). Moreover, progressive motility was higher after treatment with FF from the CTRL group as compared to the PCOS (P = 0.0029) and PCOS+Ob group (P = 0.0009). Overall, our results suggest that the FF from women with PCOS negatively impacts spermatozoa capacitation. While further studies are required to identify the molecular mechanisms, our study identified a potentially novel mechanism through which PCOS negatively impacts on fertility.