4.7 Article

Metabolic enhancement of the one carbon metabolism (OCM) in bovine oocytes IVM increases the blastocyst rate: evidences for a OCM checkpoint

Journal

SCIENTIFIC REPORTS
Volume 12, Issue 1, Pages -

Publisher

NATURE PORTFOLIO
DOI: 10.1038/s41598-022-25083-8

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Funding

  1. Iran National Science Foundation (INSF) [97002657]

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Supplementation of oocytes with metabolic enhancers of the one carbon metabolism (OCM) increases blastocyst rate in in vitro fertilization, possibly due to improved DNA methylation and epigenetic programming. The OCM supplementation enhances mitochondrial mass and DNMT3a protein expression, while reducing DNA fragmentation in matured oocytes. However, it does not directly affect the redox balance in matured oocytes. The results suggest the existence of an OCM metabolic checkpoint that hampers oocyte progression to blastocyst stage post-fertilization if not properly primed at the time of maturation.
The one carbon metabolism (OCM) has a primary role in the process of oocyte maturation. In this study bovine oocytes were cultured for 24 h, up to MII stage, with standard medium supplemented or not with 8 metabolic enhancers of the OCM and the MII and blastocyst rate were compared. Additional analyses were performed on matured oocytes, cumulus cells, zygotes and blastocysts. The OCM supplementation increased the blastocyst rate derived from in vitro fertilization. The mitochondrial mass and DNMT3a protein expression were increased whereas DNA fragmentation decreased in matured oocytes. DNA methylation in female pronucleus of zygotes was increased. The supplementation did not directly affect the redox balance as ROS and GSH in matured oocytes and homocysteine in the spent medium were unchanged. The supplementation of the oocytes with metabolic enhancers of the OCM may increase the yield from the culture, likely due to improved DNA methylation and epigenetic programming. The lack of effects on MII rate with huge differences appearing at the blastocyst stage suggest the existence of a OCM metabolic check point that hampers oocytes progression to blastocyst post-fertilization, if they were not properly primed at the time of maturation.

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