PLACENTAL TRANSPORTER ACTIVITY AND EXPRESSION IN RELATION TO FETAL GROWTH

The question of whether there are causative or compensatory changes in placental transport physiology affecting fetal growth is considered. Reductions in uterine and umbilical blood flow in growth retardation w ill reduce maternofetal exchange of lipophilic solutes, such as O-2 an d CO2, but will not have a major effect on the transfer of hydrophilic solutes. These solutes are transferred across the placenta by paracel lular diffusion, transporter protein-mediated transport and endocytosi s-exocytosis. Neither paracellular diffusion nor endocytosis-exocytosi s has been investigated in relation to fetal growth. The weight of evi dence is that there is no change in the activity and expression of the syncytiotrophoblast GLUT1 glucose transporter in fetal growth retarda tion. However, there is strong evidence that the activity of the syste m A amino acid transporter, per milligram of placental membrane protei n, is altered in relation to fetal growth, but in a complex manner. Th ere is also some weaker evidence that the activity of the Na+-H+ excha nger, per milligram of placental membrane protein, is directly related to birth-weight. There are no data for other solute transporters; a c onsiderable amount of work still remains to be done in order to unders tand the relationship between placental function and fetal growth rate .