Kurzfassung

Low levels of chronic oxidative stress are generated through expression of the cytochrome CYP2E1 in hepatocytes. This results in increased sensitivity towards cell death stimuli such as tumor necrosis factor (TNF) and can be blocked through antioxidants. Additionally the oxidative stress in these hepatocytes contributes to the modulation of insulin signalling pathways in hepatocytes characterized through inhibitory phosphorylation of the insulin receptor substrates (IRS). In hepatocytes...Low levels of chronic oxidative stress are generated through expression of the cytochrome CYP2E1 in hepatocytes. This results in increased sensitivity towards cell death stimuli such as tumor necrosis factor  (TNF) and can be blocked through antioxidants. Additionally the oxidative stress in these hepatocytes contributes to the modulation of insulin signalling pathways in hepatocytes characterized through inhibitory phosphorylation of the insulin receptor substrates (IRS). In hepatocytes these changes are blocked through inhibition of c-Jun the substrate of the mitogen-activated protein kinase (MAPK) c-Jun N-terminal kinase (JNK). The metabolic abnormalities observed in this model of chronic hepatocellular oxidative stress include a reduction in insulin-induced phosphorylation of Akt and suppression of hepatic gluconeogenesis.» weiterlesen» einklappen