Oral Presentation ESA-SRB-NZSE-CaSR 2026 in conjunction with ENSA

Impact of fatty acid transporter FATP2 deletion in male and female fertility (143698)

Morgane Goux 1 2 , Emma Cavarocchi 1 2 , Christine Légaré 1 2 , Mauro Silva 1 2 , Pierre Leclerc 1 2 , Sylvie Breton 1 2
  1. CHU de Québec-Université Laval Research Center, Quebec City, QUEBEC, Canada
  2. Centre for Research in Reproduction, Development and Intergenerational Health (CRDSI) , Quebec city, Quebec, Canada

Background: Long-chain fatty acids (LCFAs) are involved in sperm and oocyte functions. These gametes accumulate lipids during their maturation in the epididymis and ovary, respectively. During epididymal transit, spermatozoa also acquire new proteins and RNA through extracellular vesicles, called epididymosomes, which are secreted by epididymal epithelial cells. Our laboratory previously showed that one of these newly acquired proteins is the fatty acid transporter FATP2 encoded by SLC27A2 gene. As FATP2 is known to participate in the transport of LCFAs in other organs, this study aims to elucidate the role of FATP2 in the regulation of LCFAs transport in male and female fertility.

Methods: Indirect immunofluorescence staining for FATP2 was performed in mouse spermatozoa, epididymis and in the female reproductive tract. The morphology of reproductive organs as well as sperm quality parameters were compared in control mice (WT) and mice lacking the Slc27a2 gene (KO) (n≥8 mice per group).

Results: FATP2 was localized in epithelial cell apical membranes and intracellular compartments in all regions of the epididymis, oviduct and uterus. FATP2 was also detected in the sperm head, midpiece and principal piece, and in granulosa and luteal cells in the ovary. 29% (4/14) KO couples were infertile compared with 17% (1/6) WT couples. Testicular and epididymal abnormalities were observed in both strains, but with higher frequency and severity in KO mice. Spermatozoa production was significantly reduced in KO males (p=0.01), but no significant differences were observed for sperm vitality, motility, mitochondrial activity, or acrosome integrity at basal state. Surprisingly, KO spermatozoa showed fewer morphological abnormalities of the flagellar principal piece (p=0.02).

Conclusion: This study describes FATP2 localization in the female and male gametes and reproductive organs and suggests that its deletion may cause a partial infertility. We are currently evaluating female fertility and sperm functionality under capacitating conditions in KO mice.