Therefore, the predominantly diet-associated changes in PKCs levels, AKT, IKKβ, and IRS1 phosphorylation status, in conjunction with the maintained glucose muscle glucose uptake and the increased PKCε and GLUT5 protein in LBW offspring, highlight that at this young age, both WD and UPI-induced IUGR/LBW offspring present an early stage of insulin resistance pathogenesis resembling a pre-diabetic state, as described in other reports [94]. The gene discussed is AKT1; the disease is fetal growth restriction.