scholarly journals Increased sulfiredoxin-1 levels as compensatory mechanism against reactive oxygen species in women with gestational diabetes mellitus

2021 ◽  
Vol 18 (4) ◽  
pp. 267-271
Author(s):  
Burak Tatar ◽  
Uğur Turhan
Keyword(s):  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Reactive Oxygen ◽  
Compensatory Mechanism ◽  
Oxygen Species

High Glucose Level Induces Cardiovascular Dysplasia During Early Embryo Development

2017 ◽  
Vol 127 (09) ◽  
pp. 590-597
Author(s):  
Yi-mei Jin ◽  
Shu-zhu Zhao ◽  
Zhao-long Zhang ◽  
Yao Chen ◽  
Xin Cheng ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
High Glucose ◽  
Reactive Oxygen ◽  
Early Embryo ◽  
Yolk Sac ◽  
Oxygen Species ◽  
Excess Reactive Oxygen Species

AbstractThe incidence of gestational diabetes mellitus (GDM) has increased dramatically amongst multiethnic population. However, how gestational diabetes mellitus damages the developing embryo is still unknown. In this study, we used yolk sac membrane (YSM) model to investigate angiogenesis in the developing chick embryo. We determined that in the presence of high glucose, it retarded the growth and extension of the embryonic vascular plexus and it also reduced the density of the vasculature in yolk sac membrane model. Using the same strategy, we used the chorioallantoic membrane (CAM) as a model to investigate the influence of high glucose on the vasculature. We established that high glucose inhibited development of the blood vessel plexus and the blood vessels formed had a narrower diameter than control vessels. Concurrent with the abnormal angiogenesis, we also examined how it impacted cardiogenesis. We determined the myocardium in the right ventricle and left atrium were significantly thicker than the control and also there was a reduction in glycogen content in cardiomyocytes. The high glucose also induced excess reactive oxygen species (ROS) production in the cardiomyocytes. We postulated that it was the excess reactive oxygen species that damaged the cardiomyocytes resulting in cardiac hyperplasia.

Association between gestational diabetes mellitus and periodontitis via the effect of reactive oxygen species in peripheral blood cells

2021 ◽  
Author(s):  
Nattawan Bunpeng ◽  
Dittakarn Boriboonhirunsarn ◽  
Chatkoew Boriboonhirunsarn ◽  
Teerat Sawangpanyangkura ◽  
Kallapat Tansriratanawong
Keyword(s):  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Reactive Oxygen ◽  
Peripheral Blood Cells ◽  
Oxygen Species

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 Mutation at position 5628 in the mitochondrial tRNAAla gene in a Chinese pedigree with maternally diabetes mellitus

2019 ◽  
Author(s):  
Ke Li ◽  
Lijun Wu ◽  
Wei Lin ◽  
Tianlan Zhao ◽  
Qiang Qi ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Protein Synthesis ◽  
Cell Lines ◽  
Reactive Oxygen ◽  
Molecular Characteristics ◽  
Ros Generation ◽  
Oxygen Species ◽  
Cellular Models ◽  
Mitochondrial Diabetes

Abstract Background: To investigate the clinical, genetic and molecular characteristics of mitochondrial diabetes mellitus (MDM). Methods: Resultant variants were evaluated for evolutionary conservation, allelic frequencies, and structural and functional consequences. The mitochondrial function including mitochondrial tRNAAla levels, protein synthesis, membrane potential, adenosine triphosphate (ATP) production, and reactive oxygen species (ROS) generation were measured using lymphoblastoid cell lines carrying the m.5628T>C mutation and 2 controls .Results: We observed differences in the severity and age of onset in diabetes in affected maternally-related individuals, and through amolecular of the complete mitochondrial genome in this family, we identified a homoplasmic m.5628T>C mutation, located at conventional position 31 of tRNAAla, and we further detected distinct sets of mtDNA polymorphisms belonging to haplogroup L1. The identified mutation was further found be important for tRNA identity and stability. Using cellular models, we were able to determine that the respiratory deficiency caused arising as a consequence of the m.5628T>C mutation led to decreased efficiency of mitochondrial tRNAAla levels, protein synthesis, mitochondrial ATP synthesis and a reduced mitochondrial membrane potential.These mitochondrial dysfunctions caused an increase in the production of reactive oxygen species in the mutant cell lines. Conclusions: These data provide a direct evidence that novel m.5628T>C mutation may be associated with MDM, thus, offering novel insights into the understanding of pathophysiology of MDM.

Effect of reactive oxygen species overproduction on osteogenesis of porous titanium implant in the present of diabetes mellitus

Biomaterials ◽  
2013 ◽  
Vol 34 (9) ◽  
pp. 2234-2243 ◽  
Author(s):  
Ya-Fei Feng ◽  
Lin Wang ◽  
Yang Zhang ◽  
Xiang Li ◽  
Zhen-Sheng Ma ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Titanium Implant ◽  
Porous Titanium ◽  
Oxygen Species
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