In the present study, we demonstrate that 1) insulin resistance was observed in SGA rats with or without CUG, and rats with CUG show even greater insulin resistance; 2) insulin-stimulated IRS-1 and AKT phosphorylation was significantly blunted in CUG-SGA rats; 3) SOCS3 expression was upregulated in CUG-SGA rats; 4) GHR inhibition significantly suppressed SOCS3 but elevated the expression of p-IRS-1, p-AKT and p-ERK in insulin-stimulated CUG-SGA animals. The gene discussed is AKT1; the disease is Insulin resistance.