scholarly journals Evaluation of method performance for oxidative stress biomarkers in urine and biological variations in urine of patients with type 2 diabetes mellitus and diabetic nephropathy

2015 ◽  
Vol 17 (1) ◽  
Author(s):  
Ergul Belge Kurutas ◽  
Yakup Gumusalan ◽  
Ali Cetinkaya ◽  
Ekrem Dogan
2021 ◽  
Author(s):  
Sujan Banik ◽  
Antara Ghosh

Abstract Purpose: Although the exact etiologies of type 2 diabetes mellitus (T2DM) are not well defined, the effect of oxidative stress is considered an important factor in the development of T2DM. However, there are controversial outcomes in the association between oxidative stress biomarker levels and T2DM. The present study was aimed to critically examine the association of oxidative stress biomarkers with T2DM.Methods: We systematically searched different electronic databases like PubMed, Google Scholar, ScienceDirect, and Web of Science to find relevant articles up to 31 December 2019. The pooled standard mean difference (SMD) with a 95% confidence interval (CI) was used to define the variation between the study groups. Results: A total of 22 case-control studies with 2853 subjects (1667 diabetic patients and 1186 healthy controls) were selected for this meta-analysis. The pooled results of meta-analysis showed a significant difference in the malondialdehyde (MDA) levels [SMD (95% CI): 2.27 (1.62, 2.91)], nitric oxide (NO) levels [SMD (95% CI): 1.40 (0.00, 2.81)], glutathione (GSH) levels [SMD (95% CI): -1.76 (-2.94, -0.59)], and total antioxidant status (TAS) levels [SMD (95% CI): -1.40 (-2.28, -0.51)] between patients group and controls. Whereas, there was no significant difference observed in the superoxide dismutase (SOD) levels [SMD (95% CI): -1.20 (-2.55, 0.15)] and glutathione peroxidase (GPX) levels [SMD (95% CI): 0.07 (-2.80, 2.94)].Conclusion: The current meta-analysis suggests that oxidative stress might have a potential role in the pathogenesis of T2DM in humans. Further studies should be needed to elucidate the possible mechanism and strengthen this evidence.


Author(s):  
RACHNA SHARMA ◽  
SATYANARAYANA P ◽  
PALLAVI ANAND ◽  
SHRAWAN KUMAR

Objectives: Adipocytokines and oxidative stress have been independently studied in various morbidities, but their interrelationship in mediating insulin resistance and type 2 diabetes mellitus is still unclear. Thus, the present study was aimed at evaluating malondialdehyde (MDA) levels in pre-diabetes and diabetics and correlating it with adiponectin levels. Methods: Fifty controls, 50 pre-diabetic, and 50 diabetic patients were enrolled. Plasma MDA, uric acid, and adiponectin were measured in the blood samples. Serum MDA adiponectin was analyzed by enzyme-linked immunosorbent assay and uric acid was analyzed by uricase method. Results: Pre-diabetic and diabetic patients had higher levels of MDA and uric acid, while the level of adiponectin was low compared to controls. Correlation of MDA was positive with uric acid but negative with adiponectin in diabetic patients. Likewise, adiponectin and uric acid were also correlated negatively. In pre-diabetes, adiponectin was significantly and negatively correlated with MDA and uric acid. Conclusions: Pre-diabetic and diabetic patients have increased oxidative stress, which is also linked with adipokine abnormalities. From this study, we observed that oxidative stress suppresses adiponectin production which is the protective adipokine in hyperglycemia. Thus, oxidative stress may serve as an indicator or target for in the control of hyperglycemic stress.


2021 ◽  
pp. 239936932098478
Author(s):  
Joana Marques ◽  
Patrícia Cotovio ◽  
Mário Góis ◽  
Helena Sousa ◽  
Fernando Nolasco

Diabetic nephropathy is a well known complication of diabetes mellitus and the leader cause of end -stage renal disease worldwide. Nonetheless, other forms of renal involvement can occur in diabetic population. Since it has prognostic and therapeutic implications, differentiating non-diabetic renal disease from diabetic nephropathy is of great importance. We report an 80-year-old man with well-controlled type 2 diabetes mellitus and hypertension, who presented with rapid deterioration of renal function, nephrotic proteinuria, microscopic hematuria and leukocyturia. The atypical clinical presentation prompted us to perform a kidney biopsy. A diagnosis of proliferative glomerulonephritis with monoclonal immunoglobulin deposits (light chain only variant) was made, with however some chronic histological aspects which made us took a conservative therapeutic attitude. We emphasize that other causes of chronic proteinuric kidney disease should be considered in patients with type 2 diabetes mellitus, based on clinical suspicion, absence of other organ damage and mostly if an atypical presentation is seen. We review the spectrum of monoclonal gammopathies of renal significance, focusing on this rare and newly describe entity.


2021 ◽  
Vol 22 (3) ◽  
pp. 1059
Author(s):  
Bodo C. Melnik

Epidemiological studies associate milk consumption with an increased risk of Parkinson’s disease (PD) and type 2 diabetes mellitus (T2D). PD is an α-synucleinopathy associated with mitochondrial dysfunction, oxidative stress, deficient lysosomal clearance of α-synuclein (α-syn) and aggregation of misfolded α-syn. In T2D, α-syn promotes co-aggregation with islet amyloid polypeptide in pancreatic β-cells. Prion-like vagal nerve-mediated propagation of exosomal α-syn from the gut to the brain and pancreatic islets apparently link both pathologies. Exosomes are critical transmitters of α-syn from cell to cell especially under conditions of compromised autophagy. This review provides translational evidence that milk exosomes (MEX) disturb α-syn homeostasis. MEX are taken up by intestinal epithelial cells and accumulate in the brain after oral administration to mice. The potential uptake of MEX miRNA-148a and miRNA-21 by enteroendocrine cells in the gut, dopaminergic neurons in substantia nigra and pancreatic β-cells may enhance miRNA-148a/DNMT1-dependent overexpression of α-syn and impair miRNA-148a/PPARGC1A- and miRNA-21/LAMP2A-dependent autophagy driving both diseases. MiRNA-148a- and galactose-induced mitochondrial oxidative stress activate c-Abl-mediated aggregation of α-syn which is exported by exosome release. Via the vagal nerve and/or systemic exosomes, toxic α-syn may spread to dopaminergic neurons and pancreatic β-cells linking the pathogenesis of PD and T2D.


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