Control of placental glucose transfer.

There is little evidence to suggest that the membrane transfer mechanism of the placenta for glucose becomes saturated until maternal blood glucose concentrations are quite high. Also, recent evidence suggests that the membrane transport system for glucose in the placenta is not stimulated by maternal or fetal insulin. Furthermore, there is no solid evidence that hormonal or non-hormonal factors function in vivo to limit membrane transport of glucose in the placenta. Therefore, the limited data which are available suggest that there are no specific mechanisms which acutely regulate placental membrane transport of glucose, and that this membrane transport mechanism operates to maximize maternal-to-fetal glucose transfer. The rate of maternal-to-fetal glucose transfer is a function of the transplacental concentration gradient. This gradient appears to be under the control of fetal insulin and placental lactogen. The available data suggest that both hormones act to increase this concentration gradient: insulin by decreasing fetal blood glucose, and placental lactogen by both decreasing fetal and increasing maternal blood glucose concentrations. Furthermore, high rates of glucose uptake by fetal erythrocytes tend to promote maintenance of this concentration gradient. Therefore, these influences of the maternal-fetal concentration gradient promote transplacental glucose flux to the fetus. As illustrated by the fetal complications associated with maternal hyperglycaemia, the cellular and organismic physiology of the fetus and placenta appears to maximize, rather than optimize, glucose availability to the fetus. It may be, however, that during normal pregnancy, maximal availability is optimal for fetal development.