Author(s): Jansson T, Myatt L, Powell TL
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Abstract Intrauterine growth restriction (IUGR) and fetal overgrowth occur in 15\% of all pregnancies and lead to the delivery of a baby with an abnormally low or high birth weight, respectively. Both these conditions of pathological fetal growth increase the risk for perinatal complications and predispose the baby for the development of cardiovascular disease and diabetes in childhood and later in life. Fetal growth is closely related to the capacity of the placenta to transport nutrients and ions, which is dependent of the expression and activity of specific transporter proteins in the plasma membrane of the syncytiotrophoblast, the transporting epithelium of the human placenta. In human IUGR, some trophoblast nutrient and ion transporters are down regulated, whereas fetal overgrowth is associated with an up-regulation of transporters for amino acids and glucose in the placental barrier. Experimental studies have provided evidence to suggest that these changes in placental transport capacity constitute a direct cause of altered fetal growth. Therefore, regulation of placental nutrient transporters play a critical role in determining fetal growth and development, as well as the future health of the baby. This review is focused on the human and (i) summarizes the evidence that changes in the activity and expression of trophoblast nutrient and ion transporters play a central role in determining fetal growth, (ii) discusses the molecular mechanisms regulating trophoblast transporters, and (iii) highlights the implications of these findings for the development of pregnancy complications and fetal programming of cardiovascular and metabolic disease.
This article was published in Curr Vasc Pharmacol
and referenced in Pharmaceutica Analytica Acta