Moreover, oxidative stress was prominent in the juvenile female mouse model of NAFLD/NASH, and the mechanism might be related to the activation of liver NADPH oxidase.
Hence, we examined whether disruption of the redox system through a deletion of NADPH supplying mitochondrial enzyme, NADP⁺-dependent isocitrate dehydrogenase (IDH2), exacerbates fructose-induced NAFLD conditions in C57BL/6 female mice.
Association between the CYBA and NOX4 genes of NADPH oxidase and its relationship with metabolic syndrome in non-alcoholic fatty liver disease in Brazilian population.
Intestines from NAFLD mice showed higher Toll like receptor 4 (TLR4) activation and proinflammatory cytokine release, an outcome strongly dependent on the existence of NAFLD pathology and NADPH oxidase.
We hypothesized that a HFD would increase mitochondrial reliance on NAD(P)-transhydrogenase (NNT) as the source of NADPH for antioxidant systems that counteract NAFLD development.