For a long time, the study of the metabolism of nutrients by the placenta attracted
much less attention than that by the fetus. This scant interest was probably due to the
commonly held view of the placenta as an organ with minimal metabolic needs, serving
only as a means of transport between the maternal and fetal circulations. This concept
changed when it was demonstrated that in late ovine gestation only about half of the
oxygen taken up from the uterine circulation is actually delivered to the fetus whereas the
other half is used by the placenta itself, which implies a high metabolic rate
approximately equal to that of the brain. Further quantitative in vivo studies on
net substrate fluxes across both fetal and maternal circulations of the uteroplacental unit
demonstrated that placental metabolism plays a significant role in the nutritional demands
of pregnancy.
In obstetrics the main focus of scientific interest has been on the significance of
reduced uteroplacental and lUllbilical perfusion with impaired oxygenation and uptake of
nutrients as the pathophysiological mechanism of fetal growth restriction. But in smallfor-
gestational age (SGA) fetuses, not only total aminonitrogen levels are reduced, there
are also marked differences between adequate-for-gestational age (AGA) and SGA
fetuses with respect to fetal concentrations of leucine, isoleucine and valine.
A possible role for placental amino acid metabolism in fetal growth restriction is apparent
from in vivo experiments in ovine gestation with restriction of fetal growth induced by
heat-stress. These studies showed a significantly reduced uterine uptake of essential
amino acids such as threonine and leucine by the placenta expressed per gram of placenta. This finding is supported by the observation of a significantly reduced amino acid
transport activity by microvillous vesicles from placentas obtained from patients with
fetal growth restriction