It is known that fetal macrosomia is related to hyperinsulinemia during fetal development, which is a result of elevated maternal glucose concentrations which allows glucose to be transferred across the placenta, and further concentrations produced by the fetal pancreas during the second trimester, when insulin is secreted autonomously and independently of maternal glucose stimulation (Pedersen’s hypothesis) (20). This evidence concerns the gene INS and hyperinsulinism.