The management of type 2 diabetes (T2D) typically entails lifestyle modifications, including dietary adjustments and increased physical activity. However, non-pharmacological approaches alone are often insufficient for optimal control of T2D, necessitating the use of antihyperglycemic agents such as metformin, sulfonylureas, SGLT-2 inhibitors, GLP-1 agonists and others, to enhance glycemic regulation and mitigate the risk of late complications of T2D. Recent studies have increased interest in genetic polymorphisms, primarily due to their potential role in the pathogenesis of T2D. Studies show that genetic variations affect physiological mechanisms such as glucose metabolism, insulin resistance and oxidative stress regulation, which significantly influence T2D progression. Particular emphasis has been placed on polymorphisms in the KEAP1 and NFE2L2 genes, which regulate antioxidant defense mechanisms. One of the aims of our study was to determine the association between genetic variations in the KEAP1 (rs1048290 and rs9676881) and NFE2L2 (rs6706649, rs6721961, and rs35652124) genes and HbA1c levels. The study included 316 patients with T2D, where the selected polymorphisms were analyzed using the KASP method. The results showed that the presence of polymorphisms, such as KEAP1 rs9676881 and NFE2L2 rs6721961, was associated with higher HbA1c levels, indicating poorer glycemic control. In the second part of our study, we focused on the impact of genetic polymorphisms on late complications of T2D. We found that the NFE2L2 rs35652124 polymorphism was associated with an increased risk of late complications, such as ischemic heart disease, retinopathy, and nephropathy. Previous studies have confirmed this association, but they have predominantly focused on Asian populations, emphasizing the need for further research in European populations. The results of our study make an important contribution to the understanding of genetic factors influencing the development of T2D and its complications in European populations.
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