The Role of NF-κB p65 in Insulin Resistance Induced by High Glucose in 3T3-L1 Adipocytes

Abstract: This study was carried out to establish insulin-resistant cell model induced by high glucose and to investigate the effect of high glucose on NF-κB p65 expression and translocation in 3T3-L1 adipocytes . 3T3-L1 adipocytes were treated for 18 h with DMEM (1%FBS) containing 25 mmol/L glucose with or without 0.6 nmol/L insulin， or 5 mmol/L glucose with or without 0.6 nmol/L insulin. 2-deoxy-[3H]-D-glucose method was used for the determination of glucose uptake. Western blot was used for the determination of the protein expression of total NF- kB p65 and nuclear NF-κB p65. Confocal laser scanning microscope (CLSM) was used to investigate the distribution of NF-κB p65. Only in HGIns⁺ group， namely 3T3-L1 adipocytes were treated for 18 h with DMEM (1%FBS) containing 25 mmol/L glucose with 0.6 nmol/L insulin， the insulin-stimulated glucose transport of 3T3-L1 adipose cells were decreased by 55%. Both the expression of nuclear NF-κB p65 and nuclear translocation of NF-κB p65 was increased. But total NF-κB p65 protein abundance was no change during this study. These results showed only in the presence of 0.6 nmol/L insulin， high glucose can induced insulin resistance and the molecular mechanism of which might be associated with the activation and translocation of NF-κB p65.

CSTR: 32200.14.cjcb.2007.06.0019