GLUCOSE-TRANSPORTER PROTEIN EXPRESSION IN HUMAN PLACENTA THROUGHOUT GESTATION AND IN INTRAUTERINE GROWTH-RETARDATION

Despite the importance of glucose for fetal growth, gestational develo pment of placental glucose transport capacity has not been studied in the human. Furthermore, inadequate glucose transport has been implicat ed as a pathophysiological mechanism in intrauterine growth retardatio n (IUGR). We studied glucose transporter (GLUT) protein expression in sections of normal term placental tissue (immunocytochemistry) and in syncytiotrophoblast microvillous (MVM) and basal membranes (BM) isolat ed from normal term, preterm, and IUGR placentas (immunoblotting). GLU T 1, but not GLUT 3, protein was abundantly present in syncytiotrophob last membranes. MVM had similar to 3-fold higher GLUT 1 density than B M at term. MVM GLUT 1 density was maintained from 16 weeks of gestatio n to term. BM GLUT 1 density increased 2-fold in late second trimester and remained unaltered thereafter to term. GLUT 1 densities in term a nd preterm IUGR placentas were unaltered Net D-glucose uptake rates co rresponded to the GLUT 1 densities. These data suggest that 1) GLUT 1 is the main glucose transporter protein isoform in human syncytiotroph oblast; 2) the glucose transport capacity for MVM is potentially simil ar to 20-fold higher than that of BM; 3) GLUT 1 densities may be regul ated independently in MVM and BM; 4) the increase in surface area and the maintenance of a high GLUT 1 density can account for the increase in placental glucose transport in the latter part of pregnancy; and 5) fetal hypoglycemia in IUGR is not due to a decrease in placental gluc ose transporter density.