Human Reproduction, Vol. 16, No. 6, 1229-1236,
June 2001
© 2001 European Society of Human Reproduction and Embryology
Facilitated glucose transporters play a crucial role throughout mouse preimplantation embryo development
Clinic of Sterility, Department of Obstetrics and Gynaecology, University Hospital of Geneva, 1211 Geneva 14, Switzerland
The role of glucose fluctuates during preimplantation mouse embryo development, indicating that a specific interplay exists between glucose metabolism and uptake. In this study, attempts were made to characterize the role of the Na+-coupled active and the facilitated glucose transporters (GLUT) during preimplantation development by using specific glucose analogues and transport inhibitors and by examining the expression of GLUT1. One-cell outbred mouse embryos were cultured in medium M16 (5.5 mmol/l glucose), M16 without glucose (M16-G), M16-G + 2-deoxyglucose, M16-G + 3-O-methylglucose, M16 + phlorizin and M16 + phloretin and development to the blastocyst stage assessed. The absence of glucose, or the presence of 3-O-methylglucose, which is taken up but not metabolized, did not inhibit blastocyst development. 2-Deoxyglucose, which is phosphorylated but not metabolized, inhibited blastocyst development. Culture in M16 supplemented with phlorizin, an inhibitor of Na+-coupled active glucose transport did not inhibit blastocyst formation. Phloretin had no effect on the cleavage of two-cell embryos to the four-cell stage, but inhibited the morula/blastocyst transition. Both phloretin and phlorizin inhibited glucose uptake in two-cell embryos. Finally, GLUT1 expression was 10-fold less in blastocysts cultured in M16 compared to in-vivo blastocysts and those cultured in M16-G. The results show that both types of glucose transporters influence preimplantation embryo development and that the embryo has an innate ability to control the uptake of glucose by regulating the expression of GLUT1.
Key words: glucose analogues/glucose transporters/preimplantation mouse embryos
1 To whom correspondence should be addressed at: Department of Obstetrics and Gynecology, Yale University School of Medicine, 333 Cedar St, PO Box 208063, New Haven, CT 06520–8063, USA. E-mail: Denny.Sakkas{at}yale.edu
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