scholarly journals Type 1 Diabetes Mellitus in the SARS-CoV-2 Pandemic: Oxidative Stress as a Major Pathophysiological Mechanism Linked to Adverse Clinical Outcomes

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 752
Author(s):  
Aikaterini Kountouri ◽  
Emmanouil Korakas ◽  
Ignatios Ikonomidis ◽  
Athanasios Raptis ◽  
Nikolaos Tentolouris ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
B Cells ◽  
Type 1 Diabetes Mellitus ◽  
Pathophysiological Mechanism ◽  
Necrosis Factor Alpha ◽  
Angiotensin Converting Enzyme 2 ◽  
Life Threatening

Recent reports have demonstrated the association between type 1 diabetes mellitus (T1DM) and increased morbidity and mortality rates during coronavirus disease (COVID-19) infection, setting a priority of these patients for vaccination. Impaired innate and adaptive immunity observed in T1DM seem to play a major role. Severe, life-threatening COVID-19 disease is characterized by the excessive release of pro-inflammatory cytokines, known as a “cytokine storm”. Patients with T1DM present elevated levels of cytokines including interleukin-1a (IL), IL-1β, IL-2, IL-6 and tumor necrosis factor alpha (TNF-α), suggesting the pre-existence of chronic inflammation, which, in turn, has been considered the major risk factor of adverse COVID-19 outcomes in many cohorts. Even more importantly, oxidative stress is a key player in COVID-19 pathogenesis and determines disease severity. It is well-known that extreme glucose excursions, the prominent feature of T1DM, are a potent mediator of oxidative stress through several pathways including the activation of protein kinase C (PKC) and the increased production of advanced glycation end products (AGEs). Additionally, chronic endothelial dysfunction and the hypercoagulant state observed in T1DM, in combination with the direct damage of endothelial cells by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), may result in endothelial and microcirculation impairment, which contribute to the pathogenesis of acute respiratory syndrome and multi-organ failure. The binding of SARS-CoV-2 to angiotensin converting enzyme 2 (ACE2) receptors in pancreatic b-cells permits the direct destruction of b-cells, which contributes to the development of new-onset diabetes and the induction of diabetic ketoacidosis (DKA) in patients with T1DM. Large clinical studies are required to clarify the exact pathways through which T1DM results in worse COVID-19 outcomes.

Insulin Suppresses Type 1 Diabetes Mellitus-Induced Ventricular Cardiomyocyte Damage Associated with the Inhibition of Biomarkers of Inflammation and Oxidative Stress in Rats

Pharmacology ◽  
2019 ◽  
Vol 104 (3-4) ◽  
pp. 157-165 ◽  
Author(s):  
Mohammad Dallak ◽  
Bahjat Al-Ani ◽  
Dina H. Abdel Kader ◽  
Refaat A. Eid ◽  
Mohamed A. Haidara
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Serum Levels ◽  
Left Ventricular ◽  
Daily Injection ◽  
Necrosis Factor Alpha ◽  
Factor Alpha

Aims: We sought to determine whether insulin can protect against type 1 diabetes mellitus (T1DM)-induced cardiac ultrastructural alterations in an animal model of the disease. This has not been investigated before. Methods: Rats were either injected once with 65 mg/kg streptozotocin (STZ) before being sacrificed after 8 weeks or were treated with a daily injection of insulin 2 days by STZ and continued until being sacrificed. Results: Harvested tissues obtained from left ventricles in the untreated T1DM rats showed substantial damage to the cardiomyocyte ultrastructure as demonstrated by disintegrated myofibrils and their sarcomeres, damaged mitochondria and lipid droplets, which was substantially protected by insulin. Insulin also significantly inhibited T1DM-induced hyperglycemia (p < 0.001), dyslipidemia (p < 0.0001), malondialdehyde (MDA; p < 0.0001), tumor necrosis factor-alpha (TNF-α; p < 0.001) and interleukin-6 (p < 0.001). We further demonstrated a significant (p ≤ 0.001) correlation between either sarcomere or mitochondrial injury scoring and the serum levels of glucose, dyslipidemia, and biomarkers of oxidative stress (OxS) and inflammation. Conclusions: These results indicate that insulin effectively suppresses left ventricular cardiomyocyte ultrastructural damage, which substantially slows down the progression of diabetic cardiomyopathy for 8 weeks in a rat model of T1DM, possibly due to the glycemic control and inhibition of dyslipidemia, OxS and inflammation.

MULTISYSTEM INFLAMMATORY SYNDROME IN CHILDREN ASSOCIATED WITH COVID-19 IN THE 6-YEAR-OLD PATIENT WITH MANIFESTATION OF TYPE 1 DIABETES MELLITUS WITH DIABETIC KETOACIDOSIS

2021 ◽  
Vol 100 (2) ◽  
pp. 295-300
Author(s):  
Yu.V. Tikhonovich ◽  
◽  
A.Yu. Rtishchev ◽  
A.A. Glazyrina ◽  
D.Yu. Ovsyannikov ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Diabetic Ketoacidosis ◽  
Clinical Observation ◽  
Laboratory Data ◽  
Domestic Literature ◽  
Life Threatening ◽  
Inflammatory Syndrome

For the first time in the domestic literature, the article presents a clinical observation of multisystem inflammatory syndrome in children (MIS-C) associated with COVID-19 in the 6-year-old patient with manifestation of type 1 diabetes mellitus (T1DM) in the form of diabetic ketoacidosis. Anamnestic, clinical and laboratory data are presented on the basis of which two life-threatening diseases was diagnosed, as well as tactics of therapy, which made it possible to achieve a positive result. This clinical observation is compared with observations of foreign colleagues. Possible pathogenetic mechanisms of MIS-C and T1DM comorbidity are discussed.

scholarly journals Oxidative Stress in Patients with Type 1 Diabetes Mellitus: Is It Affected by a Single Bout of Prolonged Exercise?

PLoS ONE ◽  
2014 ◽  
Vol 9 (6) ◽  
pp. e99062 ◽  
Author(s):  
Maria Pia Francescato ◽  
Giuliana Stel ◽  
Mario Geat ◽  
Sabina Cauci
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Prolonged Exercise ◽  
Single Bout

scholarly journals B cells in type 1 diabetes mellitus and diabetic kidney disease

2017 ◽  
Vol 13 (11) ◽  
pp. 712-720 ◽  
Author(s):  
Mia J. Smith ◽  
Kimber M. Simmons ◽  
John C. Cambier
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
B Cells ◽  
Kidney Disease ◽  
Type 1 Diabetes Mellitus ◽  
Diabetic Kidney Disease ◽  
Diabetic Kidney

Parameters of oxidative stress in children with Type 1 diabetes mellitus and their relatives

2003 ◽  
Vol 17 (1) ◽  
pp. 7-10 ◽  
Author(s):  
Jana Varvařovská ◽  
Jaroslav Racek ◽  
František Stožický ◽  
Jiřı́ Souček ◽  
Ladislav Trefil ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus

scholarly journals Deletion of the RNLS Gene using CRISPR/Cas9 as Pancreatic Cell β Protection against Autoimmune and ER Stress for Type 1 Diabetes Mellitus

2021 ◽  
Vol 9 (F) ◽  
pp. 613-619
Author(s):  
Aufa Baraja ◽  
Fadhilla Rachmawati Sunarto ◽  
Arga Setyo Adji ◽  
Fitri Handajani ◽  
Firman Suryadi Rahman
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
B Cells ◽  
Er Stress ◽  
Type 1 Diabetes Mellitus ◽  
Genome Editing ◽  
Immune Recognition ◽  
Pancreatic Cell ◽  
The Unfolded Protein Response

BACKGROUND: Type 1 diabetes mellitus (T1DM) is a chronic disease in children which is usually caused by autoimmunity that damages pancreatic a and b cells which have functions as blood glucose regulators. Some studies stated that Renalase (RNLS) gene deletion will protect these b cells from autoimmune reactions and Endoplasmic Reticulum (ER) stress. RNLS deletion by genome editing Clustered Regular interspersed Short Palindromic Repeats-CRISPR-related (CRISPR/Cas9) is believed to have the potential to be a therapy for T1DM Patients. AIM: This research was conducted to know the potential of RNLS deletion using the CRISPR/Cas9 as an effective therapy and whether it has a permanent effect on T1DM patients. METHODS: The method applied in this research summarized articles by analyzing the titles and abstracts of various predetermined keywords. In this case, the author chose a full-text article published within the past 10 years by prioritizing searches in the last 5 years through PubMed, Google Scholar, Science Direct, Cochrane, American Diabetes Association, and official guidelines from IDAI. RESULTS: RNLS deletion using CRISPR/Cas9 in mice weakened the response of polyclonal -cell-reactive CD8+ T cells and disrupted the immune recognition to cells so that autoimmune killing did occur. In addition, such deletion prevents RNLS ER stress by increasing the threshold, triggering the unfolded protein response so that ER stress is difficult to occur. RNLS mutations in b cells also increase b cell survivability to oxidative stress. CONCLUSION: b cells RNLS deletion by genome editing CRISPR/Cas9 is effective in protecting b cells from autoimmune reactions and RE stress. However, further research is needed to determine the side effects and safety of its use.

Assessment of biomarkers of inflammation and premature atherosclerosis in adolescents with type-1 diabetes mellitus

2019 ◽  
Vol 32 (2) ◽  
pp. 109-113 ◽  
Author(s):  
Ghufran Babar ◽  
Mark Clements ◽  
Hongying Dai ◽  
Geetha Raghuveer
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Glycemic Control ◽  
Type 1 Diabetes Mellitus ◽  
Pearson Correlation ◽  
Premature Coronary Artery Disease ◽  
The Impact ◽  
Early Atherosclerosis

Abstract Background Type-1 diabetes mellitus (T1DM) causes endothelial dysfunction and early atherosclerosis, which can result in premature coronary artery disease. The aim of this study was to determine the impact of glycemic control, vascular oxidative stress and inflammation on vascular health in adolescents with T1DM. Methods This was a cross-sectional study in adolescents with age- and sex-matched T1DM who were ≥12 years and were at least 2 years post-diagnosis. Recruitment was balanced to include individuals with hemoglobin A1c (HbA1c) ≤8.5% (n=27) or with HbA1c ≥9.5% (n=25). Biomarkers of inflammation were measured in the blood including C-reactive protein (CRP), interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1), E-selectin, fibrinogen and tumor necrosis factor-α (TNF-α). Carotid intima media thickness (cIMT) and peripheral arterial tonometry (PAT) were assessed. Results Plasma E-selectin level was significantly different between the two groups with higher levels in the group with HbA1c ≥9.5% (65.0±27.7 ng/mL vs. 48.8±21.5 ng/mL, p=0.02). Though cIMT and PAT were not significantly different between the groups, Pearson correlation showed a significant direct relationship between rising HbA1c and mean right cIMT (p=0.02; r=0.37), PAT (p=0.03, r=0.31) and fibrinogen (p=0.03, r=0.03). Conclusions Elevated E-selectin level is an early marker of oxidative stress in T1DM patients with an elevated HbA1c level. Suboptimal glycemic control as evidenced by a rising HbA1c causes early atherosclerosis.

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