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- W3175226095 abstract "Type 2 diabetes (T2D) patients exhibit increased oxidative stress. However, the sources and mechanisms contributing to the elevation in oxidative stress remain unclear. Herein, we sought to examine the potential contribution of the angiotensin II-NADPH oxidase pathway in mediating the increase in oxidative stress in T2D. In 5 T2D and 5 age-matched controls, protein expression of NADPH oxidase subunits (gp91phox, p22phox, p47phox and p67phox) and angiotensin II type 1 receptor (AT1R) were assessed at rest from peripheral blood mononuclear cells using western blot. In addition, electron paramagnetic resonance (EPR) spectroscopy was used to measure blood total reactive oxygen species (ROS) and superoxide. T2D showed elevated resting total ROS (1.3±0.2×107 T2D vs. 0.6±0.1×107 controls, EPR a.u.; P<0.05) and superoxide (0.3±0.1×107 T2D vs. 0.1±0.2×107 controls, EPR a.u.; P<0.05) as well as protein expression of all NADPH oxidase subunits (P<0.05 vs. controls). AT1R expression was not different between groups. However, for all subjects, AT1R expression was significantly related to all NADPH oxidase subunits (e.g., gp91phox; R2 = 0.53; P<0.05), which in turn was related with total ROS (gp91phox; R2 = 0.59; P<0.05). These preliminary findings suggest that T2D exhibit greater ROS and superoxide that contributes to resting oxidative stress potentially via an up-regulation of the AT1R-NADPH oxidase pathway." @default.
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- W3175226095 date "2012-04-01" @default.
- W3175226095 modified "2023-10-14" @default.
- W3175226095 title "Elevated reactive oxygen species and increased mononuclear NADPH oxidase expression in type 2 diabetes patients" @default.
- W3175226095 doi "https://doi.org/10.1096/fasebj.26.1_supplement.1137.6" @default.
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