Bidirectional modulation of insulin action by reactive oxygen species in 3T3-L1 adipocytes

Reactive oxygen species (ROS) serve an important role in glucose-lipid metabolic regulation. In the present study, the results demonstrated that there was bidirectional regulation of insulin action in 3T3-L1 adipocytes treated with ROS. Transient and acute ROS exposure improved insulin-induced metabolic effects in 3T3-L1 adipocytes. Hydrogen peroxide (H(2)O(2)), as a stable and diffusible ROS, diffused into adipocytes and altered intracellular redox homeostasis, resulting in oxidation and inactivation of phosphatase and tensin homologue deleted on chromosome 10 (PTEN). Inactivation of PTEN enhanced the activation of insulin-induced protein kinase B (AKT), leading to increased glucose transporter 4 (GLUT4) redistribution and glucose uptake in 3T3-L1 adipocytes. However, chronic ROS treatment induced insulin resistance in 3T3-L1 adipocytes. It was also revealed that insulin-induced AKT activation, GLUT4 translocation to cell membrane and glucose uptake were significantly inhibited in chronic ROS-treated 3T3-L1 adipocytes. Taken together, the present study provided further demonstration that transient ROS treatment improved insulin sensitivity; however, chronic ROS exposure induced insulin resistance in 3T3-L1 adipocytes.