Abstract
The global prevalence of diabetes has increased significantly, leading to various complications and a negative impact on quality of life. Hyperglycemia hyperglycemic-induced oxidative stress (OS) and inflammation are closely associated with the development and progression of type 2 diabetes mellitus (T2D) and its complications. This review explores the effect of T2D on target organ damage and potential treatments to minimize this damage. The paper examines the pathophysiology of T2D, focusing on low-grade chronic inflammation and OS and on their impact on insulin resistance. The review discusses the role of inflammation and OS in the development of microvascular and macrovascular complications. The findings highlight the mechanisms by which inflammatory cytokines, stress kinases, and reactive oxygen species (ROS) interfere with insulin signaling pathways, leading to impaired glucose metabolism and organ dysfunction. Lifestyle interventions, including a balanced diet and exercise, can help reduce chronic inflammation and OS, thereby preventing and controlling T2D and its associated complications. Additionally, various antioxidants and anti-inflammatory agents show potential in reducing OS and inflammation. Some anti-diabetic drugs, like pioglitazone, metformin, and glucagon-like peptide-1 (GLP-1) agonists, may also have anti-inflammatory effects. Further research, including randomized controlled trials, is needed to evaluate the efficacy of these interventions.