The aim of the study was to investigate the association between lipid peroxidation and antioxidant status in nonobese type 2 diabetes mellitus (T2DM) and further to correlate whether their significant association is putatively associated with the pathogenesis of T2DM. A number of 102 nonobese T2DM subjects and 95 nondiabetic subjects as healthy controls were enrolled in this cross-sectional study. Serum samples were collected in cryovials for malondialdehyde (MDA) and thiol assays. Total thiol or sulfhydryl (–SH) groups in peripheral blood mononuclear cells (PBMCs) and sera, as well as level of MDA, a marker for lipid peroxidation in serum, were measured spectrophotometrically. Serum MDA level was found significantly higher whereas serum and PBMC total thiol levels were diminished significantly among nonobese T2DM subjects compared to HC subjects. Moreover, serum MDA level is found to have a significant inverse correlation with serum total thiol and PBMC thiol levels among DM subjects, but no significant correlation was observed in HC individuals. A significant inverse correlation between serum MDA and serum total thiol levels among nonobese T2DM subjects suggests a close association of increased oxidative stress with decreased antioxidant status in nonobese T2DM. 1. Introduction Diabetes mellitus (DM), the most common metabolic disorder worldwide and one of the leading causes of death in developed countries, is considered as a major threat to human health in the 21st century. Although the pancreatic beta-cell and its secretory product insulin are central in the pathophysiology of DM, the pathogenic mechanisms by which hyperglycemia appears differ widely. Insulin is the principal hormone that regulates uptake of glucose from the blood into most cells (primarily muscle and fat cells, but not central nervous system cells). Thus, deficiency of insulin (type 1) or the insensitivity of insulin receptors or both together (type 2) play a pivotal role in all forms of DM [1–3]. Although the causes of type 2 DM are multifactorial and include both genetic and environmental elements affecting beta-cell functions and tissue insulin sensitivity (muscle, liver, adipose tissue, pancreas, etc.), pancreatic beta-cell dysfunction and reduced insulin sensitivity are believed to play a key role in the pathogenesis of type 2 DM [3, 4]. Different studies suggest that metabolic dysregulation through oxidative stress might have an important role in the pathogenesis of DM [5]. Uncoupling of intracellular NADPH oxidase, the pivotal signaling cascade, results in the increased
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