Evaluating the Role of Trace Elements Involved in the Pathogenesis of Type 2 Diabetes Mellitus

Abstract

Type 2 diabetes mellitus is a chronic metabolic disorder specified by insulin resistance and hyperglycemia. Zinc and chromium are two examples of trace elements that are essential for many physiological and metabolic processes. The pathophysiology and consequences of type 2 diabetes (T2DM), such as retinopathy, nephropathy, neuropathy, and cardiovascular disease (CVD), may be influenced by imbalances in these components. This study sought to assess the trace element levels in T2DM patients as well as the relationship between trace elements and all clinically profiled problems. Genes impacted by trace element imbalances were found via computational analysis, and molecular docking was used to determine how these elements interacted with important proteins related to type 2 diabetes and associated consequences. Serum zinc and chromium levels were measured in a group of T2DM patients, including those without problems (retinopathy, nephropathy, CVD, and neuropathy) and those with them. The statistical studies were conducted to ascertain the significance of the variations among the groups. Furthermore, genes that could be impacted by imbalances in trace elements were found using bioinformatics methods. To investigate the binding affinities and interaction patterns of trace elements with pertinent proteins, molecular docking experiments were carried out. Trace element levels showed significant variations between T2DM patients with and without problems. More specifically, nephropathy, neuropathy, retinopathy, and CVD were shown to be more common and severe when zinc and chromium levels were lower. The hub genes that were discovered underwent computational analysis. Strong binding affinities of trace elements to important proteins involved in oxidative stress, inflammation, and insulin signaling pathways were found by molecular docking studies. The significance of trace element homeostasis in the treatment of type 2 diabetes and its consequences is highlighted by this study. The results imply that keeping an eye on and addressing trace element imbalances may lessen the likelihood and intensity of problems linked to diabetes. Insights into the genetic and molecular pathways by which trace elements impact T2DM pathophysiology can be gained through computational analysis and molecular docking, opening the door for possible therapeutic approaches that target trace element homeostasis