An Intimate Relationship between ROS and Insulin Signalling: Implications for Antioxidant Treatment of Fatty Liver Disease

Figure 1

Molecular mechanisms linking ROS, antioxidants, and the insulin signalling pathway. To allow a response to insulin stimulation, ROS are relieving insulin receptor’s inhibition by phosphatases such as PTP1B. When the cellular environment shifts to an oxidative one, because of increased mitochondrial respiration and ROS release for example, the stress-sensitive kinases are activated upon redox-sensitive phosphatases inhibition. Theses kinases are inhibiting signal amplification by inhibitory phosphorylation of IRS proteins. Mitochondrial ROS can be regulated by PGC-1𝛼-dependent detoxification system (Sirt3, SOD, GPx) or by specific mitochondrial antioxidants (SS31, MitoQ).