Diabetes mellitus is a complex metabolic syndrome characterized by a deficiency of insulin or resistance development to this hormone, leading to hyperglycemia and altered metabolism of glucose, lipids and proteins. It is considered a serious global health problem, and its complications are the major causes of morbidity and mortality in patients with the disease. From the standpoint of therapeutic methods aimed at the control of diabetes mellitus and possibly preventing its complications, treatment alternatives currently employed have focused primarily on glycemic control of patients, associated with the control of diet and physical activity. An important complication of this metabolic disease is diabetic nephropathy, characterized primarily by a progressive decline in glomerular filtration rate, persistent proteinuria and hypertension. Several mechanisms have been proposed as important in the pathogenesis and progression of diabetic nephropathy. These mechanisms include oxidative stress, lipid peroxidation and tubular damage. From this perspective, this work proposes analyses of the markers 8-oxo-2'-deoxyguanosine (8-oxodGuo), malonaldehyde (MDA) and kidney injury molecule-1 (KIM-I) over a long period of experimental diabetes without treatment and after treatment with metformin, insulin or N-acetylcysteine, in order to investigate both the likely use of these molecules as biomarkers, and the ability of these treatment strategies to modulate important biochemical pathways in the development of diabetes complications, especially diabetic nephropathy.
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