Firstly, children with IUGR show an impaired GH/IGF-I axis, which might be contributing to reduced insulin sensitivity and IGF-I resistance, as higher basal and GH-induced IGF-I levels are required to achieve a growth velocity similar to that of other children, what secondarily leads to a compensatory hyperinsulinemia to counteract insulin antagonistic effects of GH[195] and, an impaired regulation of glucose transporter-4 expression by insulin in muscle and adipose tissue[196]. This evidence concerns the gene INS and fetal growth restriction.