Development, glycolytic activity, and viability of preimplantation mouse embryos subjected to different periods of glucose starvation.
After compaction, the preimplantation mouse embryo switches to a glucose-based metabolism, whereas for the 2- to 4-cell stage embryo, glucose can be inhibitory. In this study, we investigated the adaptability of preimplantation embryos to different periods of glucose starvation by culturing in vitro fertilized (IVF) and in vivo-fertilized 1-cell OF1 mouse embryos. Blastocysts obtained from exposure to glucose starvation for different periods of time were examined for the number of cells in the trophectoderm and inner cell mass, and for glycolytic activity and viability. A high percentage of blastocysts was obtained when 1-cell embryos fertilized in vitro or in vivo were cultured in M16 until the 2-cell stage, were transferred to M16 without glucose (M16-G) until the 4- or 8-cell stage, and then were transferred to fresh M16-G. When in vivo-fertilized 1-cell embryos were cultured to the 2-cell stage and then left in M16, less than 5% formed blastocysts compared to 26% of those transferred into M16-G. Blastocysts obtained when in vivo-fertilized 1-cell embryos were left in M16-G after the 2-cell stage, however, showed a significantly elevated glycolytic activity compared to those transferred to fresh M16 or M16-G medium at the 4- or 8-cell stage. Interestingly, even though these embryos displayed elevated glycolytic activity, they did not exhibit differences in the numbers of inner cell mass and trophectoderm cells or in viability compared to embryos cultured according to other protocols. Blastocysts from all cultured protocols had a significantly lower total cell number and a lower trophectoderm, but not inner cell mass, cell number compared to blastocysts developed in vivo. This study documents the metabolic adaptability of the preimplantation embryo by highlighting its ability to proceed with development and retain viability when challenged with glucose starvation at different periods.
Leppens-Luisier
G
G
Department of Obstetrics and Gynecology, University Hospital of Geneva, Switzerland.
Sakkas
D
D
D000818:Animals; D001755:Blastocyst / Q000166:cytology / Q000378:metabolism* / Q000502:physiology; D002452:Cell Count; D002970:Cleavage Stage, Ovum / Q000502:physiology; D003470:Culture Media; D005314:Embryonic and Fetal Development / Q000502:physiology; D005260:Female; D005307:Fertilization in Vitro; D005328:Fetal Viability / Q000502:physiology*; D005947:Glucose / Q000172:deficiency*; D006019:Glycolysis / Q000502:physiology*; D051379:Mice; D011247:Pregnancy
D003470:Culture Media; D005947:Glucose