Figure 2

Short-term effects of insulin signalling and Oxidative stress. (A) Insulin (100 nM; dosing bar) activates Akt leading to Glut4 translocation and Glucose uptake (timecourses). Akt timecourse reproduces Sedaghat et al. [26]; (B) Dose response curves for bound insulin, PI3K activation and Glucose uptake; data adapted from experiments by Stagstad et al. [36] in rat adipocytes; (C) Insulin activates IRS through Tyrosine phosphorylation (IRS_Yp) and PKC inhibits through serine phosphorylation. (data adapted from experiments by Cedersund et al. [27] in human adipocytes); (D) Endogenous ROS inhibits PTP1B (data adapted from experiments by Mahadev et al. [18] in mouse 3T3-L1 adiopocytes); (E) Inhibition of NOX prevents oxidation-mediated inactivation of PTP1B and moves D-R curves of IS components to higher insulin concentrations; (F) Antioxidants control internal ROS until external ROS passes a threshold (calculations based on a model developed by Adimora et al. [35] in human Jurkat T cells); (G) ROS activates JNK/IKK; (H) Insulin (through Akt) and ROS (through JNK) modulate FOXO subcellular localization.