ObjectiveTo investigate the relationship of abnormal insulin signal transduction with NF-κB activation in the adipose tissue of patients with type 2 diabetes mellitus(T2DM),and to study the effect of NF-κB decoy on insulin resistance in vitro.MethodsDecoy targeting NF-κB was designed and synthesized.Adipocytes from abdominal subcutaneous adipose tissues were obtained from T2DM patients and non-diabetic patients.The phosphorylation of insulin signal transduction molecules IRS-1 tyrosine and Akt-Ser473 of adipocytes were examined by immunoprecipitation and Western blotting analysis after stimulation with insulin.The activity of NF-κB in the adipocytes was analyzed by electrophoretic mobility shift assay (EMSA).The NF-κB decoy was transfected into the adipocytes of T2DM patients via liposome.ResultsThe phosphorylation levels of insulin signal transduction molecule IRS-1 tyrosine and Akt-Ser473 in adipocytes T2DM patients were significantly less than that in adipocytes from non-diabetes mellitus controls(P<0.05).The activity of NF-κB in adipocytes of T2DM patients was significantly higher than that in the controls(P<0.01).After transfection of NF-κB decoy,the activity of NF-κB was decreased compared with that before transfection(P<0.05),and the phosphorylation levels of IRS-1 tyrosine and Akt-Ser473 in adipocytes of T2DM patients were significantly increased compared with those before transfection(P<0.05).ConclusionInsulin resistance and excessive activation of NF-κB exist in the adipocytes of patients with T2DM; NF-κB decoy can partly ameliorate insulin resistance.