171. PARENTAL OBESITY RETARDS EARLY EMBRYONIC DEVELOPMENT AND ALTERS CARBOHYDRATE UTILISATION

Abstract

Parental obesity impacts reproductive success and often results in gestational complications. In this study the effects of maternal and paternal obesity on preimplantation embryo quality were investigated through analysis of cell cycle length and carbohydrate utilisation. Zygotes derived from matings of lean or obese C57BL/6J mice were used to evaluate separately maternal and paternal obesity. Embryos were cultured individually, and development monitored with high temporal time-lapse microscopy (every 15 min). After 78 h of culture, glucose consumption and lactate production by expanded blastocysts was determined using ultramicrofluorimetry. Maternal obesity was associated with a significant delay (P < 0.01) in pre-compaction cell cycle length of approximately 1.5 h. Post-compaction there was a significant increase (P < 0.05) in glucose consumption by embryos from obese mothers compared to control embryos, while the glycolytic rate was unchanged. Paternal obesity was associated with a significant cell cycle delay (P < 0.05) of approximately 1h from the second cleavage stage onwards. Resultant blastocysts showed disproportionate changes in carbohydrate metabolism, with a significantly increased (P < 0.05) glycolytic rate compared to control embryos. Metabolic changes were still permissive to blastocyst formation, however cell numbers were significantly reduced (P < 0.001) with both maternal (lean: 54.2 ± 0.8 vs obese: 48.4 ± 1.0) and paternal (lean: 60.5 ± 0.09 vs obese: 50.9 ± 0.09) obesity. These data will help to determine the impact of parental obesity on preimplantation embryo physiology. Slow embryonic development and high glycolytic rate have been linked to reduced implantation rates and are general indicators of compromised embryo quality.