Peer-Reviewed Journal Details
Mandatory Fields
Higgins, BD,Kane, MT
2003
January
Reproduction
Inositol transport in mouse oocytes and preimplantation embryos: effects of mouse strain, embryo stage, sodium and the hexose transport inhibitor, phloridzin
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NEURAL-TUBE DEFECTS GLYCOSYL-PHOSPHATIDYLINOSITOL GLUCOSE TRANSPORTERS BLASTOCYSTS INVITRO RABBIT BLASTOCYSTS GENE-EXPRESSION MYOINOSITOL COTRANSPORTER CULTURE PHOSPHOINOSITIDES
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The uptake of myo-inositol by mouse oocytes and preimplantation embryos of a crossbred (DRA x C57BL/6) and a purebred outbred strain (MF1) was measured using [2-H-3]myo-inositol. Uptake in crossbred embryos increased about 15-fold between the one- and two-cell stages and increased again by about sixfold at the blastocyst stage compared with the morula stage. Uptake in purebred embryos increased about 42-fold between the one- and two-cell stages and increased more than threefold at the blastocyst stage compared with the morula stage. In all stages examined, except two-cell crossbred embryos, inositol uptake was, depending on the stage, either largely or partly sodium dependent and could be inhibited by the sodium-dependent hexose transport inhibitor, phloridzin. This is consistent with the hypothesis that transport occurs via a sodium myo-inositol transporter (SMIT) protein. in addition, there was strong evidence that a sodium-independent mechanism of uptake, possibly a channel, was switched on at the two-cell stage coincident with zygotic gene activation which resulted in 141-fold and 71-fold increases in sodium-independent uptake from the one-cell to two-cell stages in crossbred and purebred embryos, respectively. This mechanism was either abolished or drastically downregulated at the blastocyst stage, whereas sodium-dependent uptake was markedly upregulated. In two-cell crossbred embryos, there was a complete abolition of sodium-dependent uptake, again possibly regulated by zygotic gene activation. The hypothesis that the changes in mechanism of inositol uptake at about the two-cell stage are due to zygotic gene activation was supported by the finding that these changes did not occur in parthenogenetic two-cell embryos.
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