Oral Supplementation of a Standardized Naturally Fermented Papaya Preparation May Correct Type 2 Diabetes Mellitus–Induced Reactive Oxygen Species Dysregulation

2015 ◽  
pp. 490-497
Keyword(s):  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Oral Supplementation

scholarly journals Reactive Oxygen Species Modulator-1 (ROMO-1) Polymorphism Rs6060566 and The Risk of Myocardial Infarction in Slovenian Subjects With Type 2 Diabetes Mellitus

2020 ◽  
Author(s):  
Miha Tibaut ◽  
Sara Mankoč Ramuš ◽  
Daniel Petrovič
Keyword(s):  
Diabetes Mellitus ◽  
Myocardial Infarction ◽  
Reactive Oxygen Species ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Reactive Oxygen ◽  
Oxygen Species

Abstract Background We aimed to examine the role of the rs6060566 polymorphism of the reactive oxygen species modulator-1 (ROMO-1) gene in the development of myocardial infarction (MI) in Caucasians with type 2 diabetes mellitus (T2DM). Methods A total of 1072 subjects with T2DM were enrolled in cross-sectional case-control study: 335 subjects with MI and 737 subjects without clinical signs of coronary artery disease (CAD). Genetic analysis of the rs6060566 polymorphism was performed in all subjects. To assess the degree of coronary artery obstruction, a subpopulation of 128 subjects with T2DM underwent coronary computed tomography (CT) angiography. Next, endarterectomy samples were obtained during myocardial revascularization from diffusely diseased coronary arteries in 40 cases, which were analysed for ROMO-1 expression according to their genotype. Results There were no statistically significant associations between different genotypes or alleles of the rs6060566 polymorphism and MI in subjects with T2DM. The carriers of the C allele of the ROMO-1 rs6060566 had a threefold increased likelihood of having coronary artery stenosis (AOR = 3.27, 95% CI 1.16–9.20). Furthermore, the carriers of the C allele showed higher number of positive cells for ROMO-1 expression in endarterectomy samples of coronary arteries. Conclusions In accordance to our study, the rs6060566 polymorphism of the ROMO-1 gene is not the risk factor for MI in Caucasians with T2DM. However, we found that subjects carrying the C allele were at a 3.27-fold increased risk of developing severe CAD compared with those who had nonobstructive CAD. Moreover, The C allele carriers showed statistically higher number of cells positive for ROMO-1 compared with T allele carriers in coronary endarterectomy samples.

Homocysteine, reactive oxygen species and nitric oxide in type 2 diabetes mellitus

2007 ◽  
Vol 120 (4) ◽  
pp. 607-613 ◽  
Author(s):  
M.G. Signorello ◽  
G.L. Viviani ◽  
U. Armani ◽  
R. Cerone ◽  
G. Minniti ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Effects of prolonged type 2 diabetes on mitochondrial function in cerebral blood vessels

2019 ◽  
Vol 317 (5) ◽  
pp. H1086-H1092 ◽  
Author(s):  
Ivan Merdzo ◽  
Ibolya Rutkai ◽  
Venkata N. L. R. Sure ◽  
Prasad V. G. Katakam ◽  
David W. Busija
Keyword(s):  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Ros Production ◽  
Oxygen Species ◽  
Cerebral Blood Vessels

One of the major characteristics of hyperglycemic states such as type 2 diabetes is increased reactive oxygen species (ROS) generation. Since mitochondria are a major source of ROS, it is vital to understand the involvement of these organelles in the pathogenesis of ROS-mediated conditions. Therefore, we investigated mitochondrial function and ROS production in cerebral blood vessels of 21-wk-old Zucker diabetic fatty obese rats and their lean controls. We have previously shown that in the early stages of insulin resistance, and short periods of type 2 diabetes mellitus, only mild differences exist in mitochondrial function. In the present study, we examined mitochondrial respiration, mitochondrial protein expression, and ROS production in large-surface cerebral arteries. We used 21-wk-old animals exposed to peak glucose levels for 7 wk and compared them with our previous studies on younger diabetic animals. We found that the same segments of mitochondrial respiration (basal respiration and proton leak) were diminished in diabetic groups as they were in younger diabetic animals. Levels of rattin, a rat humanin analog, tended to decrease in the diabetic group but did not reach statistical significance ( P = 0.08). Other mitochondrial proteins were unaffected, which might indicate the existence of compensatory mechanisms with extension of this relatively mild form of diabetes. Superoxide levels were significantly higher in large cerebral vessels of diabetic animals compared with the control group. In conclusion, prolonged dietary diabetes leads to stabilization, rather than deterioration, of metabolic status in the cerebral circulation, despite continued overproduction of ROS. NEW & NOTEWORTHY We have characterized for the first time the dynamics of mitochondrial function during the progression of type 2 diabetes mellitus with regard to mitochondrial respiration, protein expression, and reactive oxygen species production. In addition, this is the first measurement of rattin levels in the cerebral vasculature, which could potentially lead to novel treatment options.

scholarly journals Diabetes Mellitus Directs NKT Cells Toward Type 2 and Regulatory Phenotype / Diabetes Melitus Usmerava Diferencijaciju NKT Celija U Pravcu Tip 2 I Regulatornog Fenotipa

2016 ◽  
Vol 17 (1) ◽  
pp. 35-41
Author(s):  
Nevena Gajovic ◽  
Ivan Jovanovic ◽  
Aleksandar Ilic ◽  
Nevena Jeremic ◽  
Vladimir Jakovljevic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Nkt Cells ◽  
Diabetic Patients ◽  
Oxygen Species ◽  
Chronic Disorder ◽  
Functional Phenotype

Abstract Diabetes mellitus is chronic disorder characterized by hyperglycaemia. Hyperglycaemia induces mitochondrial dysfunction, enhances oxidative stress and thus promotes reactive oxygen species (ROS) production. Earlier studies suggested that reactive oxygen species (ROS) are involved in the pathogenesis of many diseases. Previous studies have revealed that hyperglycaemia changes the functional phenotype of monocytes, macrophages, neutrophils, NK cells and CD8+ T cells. The aim of this study was to investigate whether diabetes affects the functional phenotype of NKT cells. Diabetes mellitus was induced in BALB/c mice by intraperitoneal injection of streptozotocin at a single dose of 170 mg/kg body weight. The number and functional phenotype of splenic NKT cells was assessed by fl ow cytometry, 28 days after diabetes induction. The diabetic condition facilitated the production of antioxidant enzymes, including catalase (p<0.05) and superoxide dismutase. Hyperglycaemia enhanced oxidative stress and thus decreased the number of splenic NKT cells but did not change the percentage of splenic CD3+CD49+ NKT cells that express the activatory receptor NKP46 or produce IFN-γ. However, hyperglycaemia increased the frequency of splenic NKT cells that express KLRG-1 and produce TGF-β, IL-4, and IL-5, and it decreased the frequency of IL-17+ NKT cells. Our study indicates that diabetes mellitus induces oxidative stress and switches the functional phenotype of NKT cells towards type 2 (IL-4 and IL-5 producing NKTs) and regulatory (TGF-β Thproducing NKTs) phenotypes. These findings are correlated with the clinical observation in humans that diabetic patients are more prone to infections and tumours.

scholarly journals CREBRF p.Arg457Gln Promotes Obesity and Improves Insulin Sensitivity by Promoting Preadipocyte Differentiation and Reducing Oxidative Metabolism in Gene-modified Pig Models

2021 ◽  
Author(s):  
Yingying Li ◽  
Hai Wang ◽  
Yuan Liao ◽  
Quanmei Yan ◽  
Zhen Ouyang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Oxidative Metabolism ◽  
Reactive Oxygen ◽  
Oxidative Capacity ◽  
Oxygen Species ◽  
Preadipocyte Differentiation ◽  
Human Mutation

Abstract Obesity is one of the most important risk factors for type 2 diabetes (T2DM). The CREBRF missense allele of rs373863828 (p.Arg457Gln) is associated with increased body mass index (BMI), yet reduced risk of T2DM in people with Pacific ancestry. To investigate the functional consequences of the CREBRF variant, we introduced the corresponding human mutation p.Arg457Gln into porcine genome by using a CRISPR/Cas9-mediated homologous recombination (HR)-dependent approach. The CREBRF p.Arg457Gln pig models displayed dramatically increased fat deposition, yet improved sensitivity to insulin. Transcriptome and metabolome analyses of subcutaneous white adipose tissues showed that the CREBRF p.Arg457Gln mutation promoted preadipocyte differentiation, which indicated that obesity was caused by increased number (hyperplasia) rather than size (hypertrophy) of adipocytes. In addition, the oxidative capacity decreased in the adipose tissue of pigs with CREBRF p.Arg457Gln variant. The pre-oxidative metabolite content (4-HNE and MDA) significantly decreased, while activity of antioxidant enzymes (GPX, SOD, and CAT) increased, thereby repressing oxidative metabolism of adipose tissue and reducing level of reactive oxygen species (ROS). The low reactive oxygen species could prevent insulin resistance and reduce risk of obesity-induced type 2 diabetes. This study provides further mechanistic insights into favourable adiposity resulting from CREBRF p.Arg457Gln.

Sign in / Sign up

Export Citation Format

Share Document