Ontogeny of glucose transport systems in the placenta and its progenitor tissues.

Abstract

Glucose is the primary substrate for placental and fetal metabolism, however, it can be synthesized in the fetus from placentally transferred substrates at best in minimal amounts. Therefore, the growing glucose requirements of the fetus throughout pregnancy must be met by increases in placental transport capacity. Results reviewed here indicate that the GLUT1 isoform represents the major glucose transporter species in human, and very likely in all mammalian, placentae as well as in fetal membranes and its progenitor tissues. This isoform is abundant in all placental cell populations including those fronting to the maternal and fetal circulation independent of anatomical differences of the placentae. The developmental changes of GLUT1 mRNA are controversial but the amount of GLUT1 protein tends to increase during pregnancy until term. GLUT1 seems also to play the predominant role in glucose uptake in the oocytes and preimplantation cleavage stages of rodents. Its mRNA and protein levels increased during preimplantation development. Furthermore, GLUT1 was demonstrated in the trophectoderm of mouse blastocysts, the direct progenitor tissue of the placenta. GLUT2 is generally not detected in the chorioallantoic placenta. If present at all, GLUT3 seems to be the only candidate for complementing GLUT1 in placental glucose uptake and transport function. The absence of the insulin-sensitive GLUT4 in the placenta is in line with the current consensus of insulin-independent glucose transport. The fructose transporter GLUT5 was only detected in human spermatozoa. All data available at present underline the paramount importance of GLUT1 for glucose transfer in the developing fetoplacental unit.