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.

Dihydromyricetin regulates RIPK3-CaMKII to prevent necroptosis in high glucose-stimulated cardiomyocytes

“…High glucose augments ROS generation and impairs mitochondrial function and structure, as reflected by reduction in mitochondrial membrane potential (Δψm) [ 21 , 22 ]. JC-1 staining found that the green fluorescence intensity (GFI) of the JC-1 monomers, representing depolarized Δψm, was increased after HG stimulation.…”

Genetic and Transcriptomic Background of Oxidative Stress and Antioxidative Therapies in Late Complications of Type 2 Diabetes Mellitus: A Systematic Review

“…As a carotenoid, it contains four major components, which are crocin, crocetin, picrocrocin, and safranal. In addition to the direct antioxidative effect, carotenoids also activate Nrf2, a master regulator gene that activates genes, involved in the oxidative stress response [ 23 ]. A recent 90-day trial (15 mg of crocin/day) in a group of T2DM patients with microalbuminuria showed that crocin reduced body mass index (BMI) and systolic and diastolic blood pressure.…”

“…It is widely acknowledged that genetic variability, as well as environmental factors, including modifiable lifestyle factors such as diet, influence the activity and/or the expression levels of oxidative-stress-related enzymes, thus, contributing to the individual differences observed in antioxidant defense mechanisms and susceptibility to oxidative stress [ 20 ]. Therefore, genetic variability and alterations in gene expression levels may also play a role in the development of T2DM late complications [ 21 , 22 , 23 ].…”

Effect of GLP-1 Receptor Agonist on Ischemia Reperfusion Injury in Rats with Metabolic Syndrome

“…Oxidative stress, usually defined as a discrepancy in the production and elimination of reactive species (mostly oxygen, but also nitrogen, sulfur or carbon), in favor of their accumulation, has a key role in many CVD [ 14 ]. Oxidative stress in diabetes and MetS is additionally augmented, which is why it is one of the key factors for the development of cardiovascular complications associated with impaired glucoregulation [ 15 ]. Oxidative stress is in close relation to inflammation.…”