Our studies show that an increase in circulating maternal testosterone levels in pregnant rats at a clinically relevant concentration (2-fold--similar to that observed in human pregnancies complicated with IUGR [6-10]) induced fetal growth restriction without increase in fetal testosterone levels, but it is associated with a reduction in placental amino acid transport activity, possibly through a decrease in expression of the slc38a2/Snat2 amino acid transporter. This evidence concerns the gene SLC38A2 and fetal growth restriction.