Oxidative Stress in Type 2 Diabetes: Impacts from Pathogenesis to Lifestyle Modifications

Abstract

Oxidative stress is a critical factor in the pathogenesis and progression of diabetes and its associated complications. The imbalance between reactive oxygen species (ROS) production and the body's antioxidant defence mechanisms leads to cellular damage and dysfunction. In diabetes, chronic hyperglycaemia and mitochondrial dysfunction contribute to increased ROS production, further exacerbating oxidative stress. This oxidative burden adversely affects various aspects of diabetes, including impaired beta-cell function and insulin resistance, leading to disrupted glucose regulation. Additionally, oxidative stress-induced damage to blood vessels and impaired endothelial function contribute to the development of diabetic vascular complications such as retinopathy, nephropathy, and cardiovascular diseases. Moreover, organs and tissues throughout the body, including the kidneys, nerves, and eyes, are vulnerable to oxidative stress, resulting in diabetic nephropathy, neuropathy, and retinopathy. Strategies to mitigate oxidative stress in diabetes include antioxidant therapy, lifestyle modifications, and effective management of hyperglycaemia. However, further research is necessary to comprehensively understand the underlying mechanisms of oxidative stress in diabetes and to evaluate the efficacy of antioxidant interventions in preventing and treating diabetic complications. By addressing oxidative stress, it might be possible to alleviate the burden of diabetes and improve patient outcomes.

Keywords: Mediterranean diet; diabetes complications; diet; lifestyle modifications; oxidative stress; physical activity; type 2 diabetes.

Figure 1

Main pathophysiological mechanism of hyperglycaemia induced oxidative stress. Abbreviations: PKC—Protein Kinase C and AGEs—advanced glycation end products.

Figure 2

Mediterranean diet nutrients that exert an anti-inflammatory and antioxidant effect.

Figure 3

Oxidative stress and antioxidant imbalance due to physical exercise. Abbreviations: XO—xanthine oxidase, eNOS—endothelial nitric oxide synthase, nNOS—neural nitric oxide synthase, NOX2—NADPH oxidase-2, PLA2—phospholipase A2, GSH—glutathione, nrf2—nuclear factor erythroid 2-related factor 2, SOD—superoxide dismutase, CAT—catalase, and GPx—glutathione peroxidase.