Adaptations in placental nutrient supply capacity to meet fetal demand: implications for intrauterine programming

Abstract

Fetal growth is absolutely dependent on supply of nutrients from mother via the placenta. A variety of human and mouse data together suggest that placental capacity to supply nutrient is adaptable in relation to fetal demand. (1) In normal human pregnancy the activity, per mg membrane protein, of the System A amino acid transporter in the microvillous plasma membrane (MVM) of the placental syncytiotrophoblast is inversely related to the birthweight and size of baby. (2) In mice with a deletion of the placental transcript of the insulin‐like growth factor 2 (igf2) gene, placental weight is reduced compared to wild type mice at e16 (term e20) but fetal weight is not reduced at this time, perhaps because System A expression and activity, per g placenta, is higher in the knockout conceptuses. (3) In the same knockout mice fetal calcium accretion is reduced compared to wild type at e17, but returns to normal by e19 apparently through an increased activity/expression of placental calcium transport mechanisms. (4) Most recently, we find apparent adaptations in placental transporter and vascular reactivity in pregnancies complicated by obesity and pre‐eclampsia respectively. The variable nature of the placental transfer adaptations in different situations, as found in these different studies, will variably affect the mix of nutrient transferred and so potentially variably programme fetal homeostatic mechanisms.