While these results do not support an important role for SLC2A8 in placental glucose transport, culturing murine embryos with Slc2A8 antisense RNA resulted in increased blastocyst apoptosis and reduced viability [20], and Limesand et al. [23] reported diminished placental expression of SLC2A8 in a sheep model of placental insufficiency resulting in intrauterine growth restriction (IUGR). This evidence concerns the gene SLC2A8 and fetal growth restriction.