Essential role of glucose transporter GLUT3 for post-implantation embryonic 
development

Schmidt, S.; Hommel, A.; Gawlik, V.; Augustin, R.; Junicke, N.; Florian, S.; Richter, M.; Walther, D. J.; Montag, D.; Joost, H.-G.; Schürmann, A.

doi:10.1677/JOE-08-0262

Item

ITEM ACTIONSEXPORT

Add to Basket

Local TagsRelease HistoryDetailsSummary

Released

Journal Article

Essential role of glucose transporter GLUT3 for post-implantation embryonic development

MPS-Authors

/persons/resource/persons50622

Walther, D. J.
Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society;

External Resource

No external resources are shared

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

Fulltext (public)

There are no public fulltexts stored in PuRe

Supplementary Material (public)

There is no public supplementary material available

Citation

Schmidt, S., Hommel, A., Gawlik, V., Augustin, R., Junicke, N., Florian, S., et al. (2009). Essential role of glucose transporter GLUT3 for post-implantation embryonic development. Journal of Endocrinology, 200(1), 23-33. doi:10.1677/JOE-08-0262.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0010-7E53-F

Abstract

Deletion of glucose transporter gene Slc2a3 (GLUT3) has previously been reported to result in embryonic lethality. Here, we define the exact time point of growth arrest and subsequent death of the embryo. Slc2a3–/– morulae and blastocysts developed normally, implanted in vivo, and formed egg-cylinder-stage embryos that appeared normal until day 6.0. At day 6.5, apoptosis was detected in the ectodermal cells of Slc2a3–/– embryos resulting in severe disorganization and growth retardation at day 7.5 and complete loss of embryos at day 12.5. GLUT3 was detected in placental cone, in the visceral ectoderm and in the mesoderm of 7.5-day-old wild-type embryos. Our data indicate that GLUT3 is essential for the development of early post-implanted embryos.