Abstract:

Oxidative stress is an important player that can play a role in both the formation of type 2 diabetes and the development of diabetes complications. Basically, oxidative stress is used in the definition of the physiological condition resulting from a disbalance between the formation of reactive oxygen derivatives (ROS) and disbalance. Data obtained from clinical studies show that systemic oxidative stress is closely related to metabolic syndrome and components. Chronic hyperglycemia and hyperlipidemia are important risk factors for the formation of ROS. The contribution of hyperglycemin to the accumulation of ROS can occur through different metabolic pathways. Basically, the increase in the activity of the glycolytic pathway in hyperglycemic conditions and the electron pressure on the mitochondrial electron transmission system contribute to the formation of ROS. The formation and accumulation of reactive oxygen derivatives subsequently pushes the activity of the enzyme glyceraldehyde 3-P dehydrogenase (GAPDH) from the key enzymes responsible for glycolis, forcing the cell to metabolize glucose with alternative pathogens. The effectiveness of the glucose and cancer cycle is reduced; the polyol pathway, the hexosamine pathway and the protein kinase C (PCK) activity is increased. All of these alternative metabolic drops further increase the formation of ROS in the cell. ROS accumulation can contribute to insulin resistance pathogenesis by reducing insulin genetic expression and insulin release from beta cells through posttranslation factors. ROS accumulation caused by hyperglycemia also plays an important role in the formation of diabetes complications. The results of clinical trials show that many indicators can be used to determine the oxidative damage caused by diabetes and complications in the protein, lipid and nucleic acid components of the cell, and that these indicators can give an idea of the level of oxidated acid.

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