Fetal Liver and the Placenta: An Interactive System

Fetal physiologists have centered their attention on the endocrine system when considering the potential interaction of one fetal organ with another or one fetal organ with the placenta. Our own studies in pregnant sheep showed an impressive correlation between placental size and the size of the fetal liver (Fig. 1). This observation—which is not a characteristic of the fetal brain, for example—suggests that the growth of the two organs is interrelated. In our earlier studies of carbohydrate metabolism, it rapidly became clear that the function of the fetal liver and the placenta must be integrated, at least with respect to glucose metabolism. In a series of studies (1-3), we showed that the placental delivery of glucose to the fetus was a function of the transplacental glucose gradient. The fetal hepatic production of glucose was also a function of the placental delivery of glucose. Only when the latter fell to low levels did the rate of fetal gluconeogenesis become significant (3). This makes good sense, of course, because if the fetal liver constantly produced glucose, it would decrease the transplacental gradient by raising fetal glucose concentration. This would then lead to reduced umbilical uptake. Hence, fetal hepatic glucose production, under normal circumstances, would be counterproductive, as it would substitute fetal carbon sources for maternal glucose carbon. These studies made us curious as to whether a similar interaction between fetal hepatic metabolism and placental transport and metabolism also existed for amino acids.