scholarly journals Assessment of oxidative stress and endothelial dysfunction in Asian Indians with type 2 diabetes mellitus with and without macroangiopathy

QJM ◽  
2008 ◽  
Vol 101 (6) ◽  
pp. 449-455 ◽  
Author(s):  
N. Singhania ◽  
D. Puri ◽  
S.V. Madhu ◽  
S.B. Sharma
PLoS ONE ◽  
2014 ◽  
Vol 9 (11) ◽  
pp. e108587 ◽  
Author(s):  
Pawel P. Wolkow ◽  
Wladyslaw Kosiniak-Kamysz ◽  
Grzegorz Osmenda ◽  
Grzegorz Wilk ◽  
Beata Bujak-Gizycka ◽  
...  

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Shuai Huang ◽  
Gen Chen ◽  
Jia Sun ◽  
Yunjie Chen ◽  
Nan Wang ◽  
...  

Abstract Background The mechanism underlying endothelial dysfunction leading to cardiovascular disease in type 2 diabetes mellitus (T2DM) remains unclear. Here, we show that inhibition of histone deacetylase 3 (HDAC3) reduced inflammation and oxidative stress by regulating nuclear factor-E2-related factor 2 (Nrf2), which mediates the expression of anti-inflammatory- and pro-survival-related genes in the vascular endothelium, thereby improving endothelial function. Methods Nrf2 knockout (Nrf2 KO) C57BL/6 background mice, diabetic db/db mice, and control db/m mice were used to investigate the relationship between HDAC3 and Nrf2 in the endothelium in vivo. Human umbilical vein endothelial cells (HUVECs) cultured under high glucose-palmitic acid (HG-PA) conditions were used to explore the role of Kelch-like ECH-associated protein 1 (Keap1) –Nrf2–NAPDH oxidase 4 (Nox4) redox signaling in the vascular endothelium in vitro. Activity assays, immunofluorescence, western blotting, qRT-PCR, and immunoprecipitation assays were used to examine the effect of HDAC3 inhibition on inflammation, reactive oxygen species (ROS) production, and endothelial impairment, as well as the activity of Nrf2-related molecules. Results HDAC3 activity, but not its expression, was increased in db/db mice. This resulted in de-endothelialization and increased oxidative stress and pro-inflammatory marker expression in cells treated with the HDAC3 inhibitor RGFP966, which activated Nrf2 signaling. HDAC3 silencing decreased ROS production, inflammation, and damage-associated tube formation in HG-PA-treated HUVECs. The underlying mechanism involved the Keap1–Nrf2–Nox4 signaling pathway. Conclusion The results of this study suggest the potential of HDAC3 as a therapeutic target for the treatment of endothelial dysfunction in T2DM.


Author(s):  
Siva Prasad Palem

Objective: To evaluate the correlation of uric acid with oxidative stress and endothelial dysfunction in type 2 diabetic subjects.Material and Methods: The study included 120 subjects, among when 60 were type 2 diabetes subjects and the remaining 60 were age and gender matched healthy controls. The biochemical parameters, blood glucose, lipid profile, uric acid and homocysteine, were measured by standard kits in an autoanalyzer. Oxidative stress was evaluated by measuring malondialdehyde (MDA) and total antioxidant power by manual methods such as thio-barbituric acid reactive substances and ferric reducing ability of plasma (FRAP). Endothelial dysfunction was assessed by measuring nitric oxide (NO) by the kinetic cadmium method.Results: A significant elevation of triglycerides, low density lipoprotein (LDL), and MDA were observed in the type 2 diabetes mellitus patients while FRAP and NO were significantly reduced compared to the healthy controls. In addition, the uric acid levels had a highly significant correlation with FRAP (r=0.212, p-value=0.020), and moderately significant correlation with triglycerides (r=0.173, p-value=0.057) and homocysteine (r=0.178, p-value=0.051). Uric acid was negatively correlated with MDA and positively correlated with NO, but not statistically significant.Conclusion: Our findings suggest that uric acid may have antioxidant properties since it had a significant positive correlation with FRAP.


2020 ◽  
Vol 101 (1) ◽  
pp. 13-17
Author(s):  
F I Mammadova

Aim. To estimate the severity of endothelial dysfunction and effects of nitric oxide, thiol status and cystatin on the progression of chronic heart failure and chronic heart failure in type 2 diabetes mellitus. Methods. 80 patients (men and women) with chronic heart failure were included. All patients were divided into two groups: the first group 39 patients with chronic heart failure, the second 41 people with chronic heart failure and type 2 diabetes mellitus. The control group consists of 20 healthy donors. To obtain statistically significant differences with the control group the minimum sample size for observations was determined based on the target variance of a small sample (n=10). The lipid profile and carbohydrate metabolism, endothelin-1, cystatin, nitric oxide were evaluated. Statistical processing was performed using Microsoft Office Excel and IBM SPSS Statistics 20 software. Results. Changes in lipid metabolism were found in both groups, while an increase in carbohydrate metabolism was observed in patients with chronic heart failure with type 2 diabetes mellitus. Under conditions of oxidative stress in patients with chronic heart failure, a decrease in the content of thiol status and an increase in the amount of nitric oxide in the blood serum were recorded. The endothelin-1 level was elevated, particularly in the second group, which indicates a more serious endothelial dysfunction with increased glucose content in patients with chronic heart failure. Conclusion. The level of cystatin C as an atherogenic risk factor was equally increased in the studied patients, possibly it affected by the rate of disease progression; feasible to use these markers to detect the progression of chronic heart failure in the early stages.


2020 ◽  
Author(s):  
P. Siva Prasad ◽  
P. Hari Prasad ◽  
T. Sudhakar ◽  
B. Rajkumar ◽  
Adithya Raj ◽  
...  

Abstract Objective: Uric acid is an end product of purine metabolism and it has two different functions such as pro-oxidant and anti-oxidant. Where, pro-oxidant and anti-oxidants are opposite in action. Oxidative stress and endothelial dysfunction are a foremost cause of complications in diabetes mellitus, where uric acid may play a major role in this process. Hence, the present study has been designed to evaluate antioxidant activity of uric acid and its correlation with oxidative stress and endothelial dysfunction in type 2 diabetic subjects. Methods: We included 120 subjects in this study with age group of 39 -60 years. Among these 60 were type 2 diabetic subjects and 60 were healthy controls. The estimation of biochemical parameters such as blood sugar, lipid profile, uric acid, and homocysteine are measured in fully auto-analyzer with well recognized methods. MDA measured by TBARS method, total antioxidant capacity as FRAP and NO estimated by Kinetic cadmium method in spectrophotometer. Results: The study was found significant elevation of triglyceride, LDL and MDA and significant lower level of FRAP and NO in T2DM than healthy control. Uric acid was insignificant in T2DM compared to healthy control. However, uric acid has significant correlation with FRAP (r=0.2116, p=0.02) and moderate correlation with triglyceride (r=0.1736, p=0.0579) and homocysteine (r=0.1779, p=0.0519). MDA was negatively and NO was positively correlated with uric acid but statistically insignificant. Conclusion: We have found antioxidant activity of uric acid where it was determined by significant positive correlation with FRAP in type 2 diabetes mellitus.


Author(s):  
Nermien Abd El Rahman Ibraheim ◽  
Fatema El Zahraa Sayed Bukhary ◽  
Yehia Zakareia Mahmoud ◽  
Mahmoud Ragab Mohamed ◽  
Salama Rabei Abdel-Rahim

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.


Sign in / Sign up

Export Citation Format

Share Document