Abstract

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.

Highlights

  • 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

  • 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

  • Serum MDA level was found significantly higher among nonobese DM subjects compared to healthy control (HC) individuals (3.21 ± 1.84 versus 2.05 ± 0.99 nmol/L; P < 0.0001) (Figure 1), whereas serum and peripheral blood mononuclear cells (PBMCs) total thiol levels were diminished significantly among DM subjects compared to HC subjects

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Summary

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. 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]. Oxidative stress develops in diabetes due to poor elimination of ROS from different tissues [6, 7]. Oxidation of complex lipids in vivo is largely caused by ROS such as hydroxyl radical, which in turn are synthesized by lipoxygenases as a response to cell injury, typically from hydrogen peroxide. The major targets of these damaging species are the long-chain polyunsaturated

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