Oxidative stress is a significant contributor to the onset and progression of diabetes and its complications. It leads to insulin resistance, β-cell dysfunction, impaired glucose tolerance, and mitochondrial dysfunction. Experimental and clinical data suggest an inverse relationship between insulin sensitivity and reactive oxygen species (ROS) levels. Oxidative stress can arise from various sources, including ketosis, sleep restriction, and excessive nutrient intake. It activates stress pathways involving serine/threonine kinases, which negatively affect insulin signaling. More research is needed to identify the mechanisms contributing to insulin resistance in both type 1 and non-diabetic individuals. Reducing hyperglycemia and calorie intake can control oxidative stress. This review outlines the mechanisms leading to oxidative stress and suggests that interventions and therapies targeting these mechanisms may reduce the risk of insulin resistance and diabetes.Oxidative stress is a significant contributor to the onset and progression of diabetes and its complications. It leads to insulin resistance, β-cell dysfunction, impaired glucose tolerance, and mitochondrial dysfunction. Experimental and clinical data suggest an inverse relationship between insulin sensitivity and reactive oxygen species (ROS) levels. Oxidative stress can arise from various sources, including ketosis, sleep restriction, and excessive nutrient intake. It activates stress pathways involving serine/threonine kinases, which negatively affect insulin signaling. More research is needed to identify the mechanisms contributing to insulin resistance in both type 1 and non-diabetic individuals. Reducing hyperglycemia and calorie intake can control oxidative stress. This review outlines the mechanisms leading to oxidative stress and suggests that interventions and therapies targeting these mechanisms may reduce the risk of insulin resistance and diabetes.