Placental nutrient transfer and fetal growth

Abstract

The placenta represents the interface between the mother and fetus and delivers all the nutrients necessary for normal fetal growth and development. Consequently, fetal growth is intimately linked to the transport functions of the placenta. Two important pregnancy complications are associated with altered fetal-growth patterns. In intrauterine growth restriction (IUGR), the fetus fails to achieve its genetically determined growth potential and is born with a low birth weight for gestational age. In contrast, some fetuses of mothers with diabetes represent the other end of the growth spectrum in displaying signs of fetal overgrowth. Historically, the restricted growth in IUGR has been attributed to reduced placental blood flow, and the accelerated fetal growth in some diabetic pregnancies has been explained by maternal hyperglycemia. However, a growing body of evidence is now available suggesting that alterations in the activity and expression of placental nutrient transporters may contribute to the development of these pregnancy complications. In the human placenta there are two cell layers positioned between the maternal and fetal blood circulations: the syncytiotrophoblast and the fetal capillary endothelium. For the primary fetal nutrients, such as glucose and amino acids, the plasma membranes of the syncytiotrophoblast cell constitutes the main barrier for transplacental transport. The syncytiotrophoblast is a true syncytium with polarized plasma membranes: the microvillous membrane (MVM) faces the maternal blood and the basal membrane (BM) is adjacent to the fetal capillary. As in other epithelial cells, differences in the type, number and activity of transporters in these two plasma membranes of the syncytiotrophoblast provide the basis for vectorial transport of nutrients. Thus, isolation of MVM and BM and the subsequent study of these membrane fractions in vitro is a valuable strategy to assess placental transport functions of the human placenta.