Although we have shown that the pharmacological activation of AMPK by MET lowers the blood glucose level and improves intrauterine fetal growth in murine models of GDM, the contribution of trophoblastic GLUT3 to the amelioration of hyperglycemia remains unclear because the administration of MET might also lower the circulatory glucose levels by simultaneously enhancing the GLUT4-mediated uptake of glucose in skeletal muscle cells. This evidence concerns the gene SLC2A3 and gestational diabetes.