Are oxidative stress-activated signaling pathways mediators of insulin resistance and beta-cell dysfunction?

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Molecular Mechanisms Linking Oxidative Stress and Diabetes Mellitus (2020, background): “Moreover, a wide range of oxidative stress-induced factors and byproducts such as p38 MAPK, JNK/SAPK, PKC (protein kinase C), sorbitol, and hexosamine are all activated by oxidative damage and can suppress GLUT-4 expression [29].”
Beta Cell Dysfunction and Insulin Resistance (2013, background): “This infers that beta cell function supersedes insulin resistance as the critical determinant of type 2 diabetes.”
Mitochondrial Fission Contributes to Mitochondrial Dysfunction and Insulin Resistance in Skeletal Muscle (2011, background): “No difference in the phosphorylation of JNK was detectable among the three groups.”
Mechanisms of obesity-associated insulin resistance: many choices on the menu. (2007, background): “Many of the human studies on the link between oxidative stress and insulin resistance focus on the generation of ROS by hyperglycemia in diabetic patients, implicating ROS as a consequence of diabetes-induced hyperglycemia and not a causative factor for insulin resistance (Evans et al. 2002, 2003).”
Diabetes associated cell stress and dysfunction: role of mitochondrial and non‐mitochondrial ROS production and activity (2007, background): “The high degree of oxidative stress has been postulated to play an important role in decreasing insulin responsiveness (Evans et al. 2003; Urakawa et al. 2003).”