In the placenta, although post-receptor defects have been recognized in the insulin signaling pathway in non-obese and obese women with insulin-controlled GDM, a controversy still exists about changes in the expression of placental glucose transporter isoforms 1 (insulin-independent GLUT1), 3 (GLUT3 being a high-affinity glucose transporter), and 4 (insulin-dependent GLUT4), encoded by the SLC2A1, SLC2A3, and SLC2A4 genes, respectively, and their roles in disturbances in transplacental energy substrate supply in diabetic pregnancy [5,7,8,9,10]. This evidence concerns the gene SLC2A3 and gestational diabetes.