Therefore, a potential explanation for the observed results is that the “energy” economy mode adopted by the IVP embryos [72], and the subtle but impaired placental perfusion during pregnancy, impacted the liver metabolism during fetal life, increasing glucose production from the liver and leading to increased peripheral insulin sensitivity in postnatal life, in a similar fashion as occurring in IUGR fetuses [73]. This evidence concerns the gene INS and fetal growth restriction.