scholarly journals Relationship between Type 2 Diabetes and Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency and Their Effect on Oxidative Stress

2018 ◽  
Vol 09 (08) ◽  
Author(s):  
Godwill Azeh Engwa ◽  
Friday Nweke Nwalo ◽  
Gregory Eze Chibuzor ◽  
Endaline Chiamaka Ejiagha ◽  
Micheal Chinweuba Abonyi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
G6pd Deficiency ◽  
Glucose 6 Phosphate Dehydrogenase

scholarly journals SARS-CoV-2 Trigger in Severe Insulin Resistance With Acute Haemolytic Crisis in Diabetes and Glucose-6-phosphate Dehydrogenase Deficiency

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A397-A398
Author(s):  
Hareesh Joshi ◽  
Kenneth Earle
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
G6pd Deficiency ◽  
Insulin Infusion ◽  
Once Daily ◽  
Acting Insulin ◽  
History Of ◽  
Glucose 6 Phosphate Dehydrogenase

Abstract Background: We report a case of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection as trigger for increased insulin resistance and severe haemolytic crisis in a male with type 2 diabetes mellitus and glucose-6-phosphate dehydrogenase (G6PD) deficiency. Clinical Case: A 64-year-old man (BMI 25kg/m2, weight 75kg) with past medical history of type 2 diabetes mellitus (on metformin and sitagliptin; glycated haemoglobin 51 mmol/mol, n<42mmol/mol), hypertension, G6PD deficiency and gout was admitted to hospital with COVID pneumonitis and type 1 respiratory failure giving 5 days’ history of cough, shortness of breath, fatigue and tiredness. As per hospital guidelines, the patient was treated with amoxicillin/clavulanate 625mg three times daily and doxycycline 100mg once daily. Hydroxycholoroquine was not given in view of G6PD deficiency. There was no evidence of diabetic ketoacidosis and a short-acting insulin sliding scale was initiated at 2U/hr. Continuous positive pressure ventilation was offered for next 72 hours, however the patient failed to improve and required transfer to intensive care unit for intubation and mechanical ventilation. Computer tomography scan of pulmonary artery excluded embolism. The patient was fed via nasogastric tube post intubation. On day 8, the patient experienced a sudden drop in haemoglobin levels from 132 g/dl on day 1 to 68 g/dl, requiring multiple blood transfusions. The blood results demonstrated evidence of haemolysis with a rise in total and direct bilirubin and lactate dehydrogenase levels. The peripheral blood smear showed numerous bite cells with polychromasia suggesting an acute haemolytic crisis in the context of G6PD deficiency. A medication review revealed no evidence of drug-induced haemolysis. Later the patient was started on dexamethasone 6mg once daily (day 11) and on remdesivir 100mg once daily (day 15). During this time, the patient’s insulin infusion requirements had progressively increased from 2U/hr to 8U/hr (equivalent to 192 units/24 hr). On day 22, the patient’s clinical condition deteriorated with septicaemia requiring extended course of antibiotics. At this time, continuous insulin infusion was stopped and intermediate acting insulin (insulatard 36U twice daily; later increased to 48U twice daily) was started. In the next 10 days, the patient made good clinical recovery from sepsis with stable haemoglobin and blood sugar levels. He was extubated and transferred for rehabilitation. The patient was successfully weaned off insulin in the community with optimal diabetes control. Conclusion: This is a case demonstrating the possible role of SARS-CoV-2 in increased insulin resistance and severe haemolytic crisis on background of diabetes and G6PD deficiency.

scholarly journals Glucose-6-Phosphate Dehydrogenase (G6PD) status in Female Type 2 Diabetes Mellitus and its Relationship with HbA1C

1970 ◽  
Vol 5 (2) ◽  
pp. 60-65 ◽  
Author(s):  
Nadira Akter ◽  
Noorzahan Begum ◽  
Sultana Ferdousi
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Risk Factor ◽  
G6pd Deficiency ◽  
Glycosylated Hemoglobin ◽  
Health Science ◽  
Control Group ◽  
Glucose 6 Phosphate Dehydrogenase

Background: Glucose-6-phosphate dehydrogenase (G6PD) deficiency may be one of the risk factor for type 2 diabetes mellitus. Objective: To observe erythrocyte G6PD status in type 2 female diabetic patients and also to find out its relationship with glycosylated hemoglobin. Methods: This cross sectional study was carried out in the Department of Physiology, Bangabandhu Sheikh Mujib Medical University, Shahbag, Dhaka from January to December 2009. For this, 60 female patients with type 2 diabetes mellitus, age ranged from 40 to 60 years were included in the study group (group B). On the basis of glycosylated hemoglobin level (HbA1C) they were further subdivided into group B1, consisting of 30 controlled diabetics (HbA1C 4.8-6%) and group B2, consisting of 30 uncontrolled diabetic (HbA1C>6%) patients. They were selected from Out Patient Department of Bangladesh Institute of Health Science Hospital. For comparison, age & sex matched 30 apparently healthy non diabetic females (group A) were also studied. Erythrocyte G6PD level was measured by Spectrophotometer, HbA1C level by Flex reagent cartridge and serum bilirubin, Hb%, total count of RBC and reticulocyte% were measured by standard laboratory techniques. For statistical analysis ANOVA, independent sample t test, χ2 test and Pearson's correlation coefficient test were performed as applicable. Results: In this study, erythrocyte G6PD level was significantly lower in both the diabetic groups (p <0.001) than those of control group but their difference when compared between B1 and B2 was not statistically significant. In controlled diabetics 20% and in uncontrolled diabetics 6.7% patients were found G6PD deficients. No G6PD deficient subjects were found in control group. HbA1C showed negative correlation with Erythrocyte G6PD which was only significant for uncontrolled diabetes (p < 0.05) Conclusion: This study concludes that G6PD deficiency may be one of the risk factor for type 2 diabetes mellitus irrespective of blood glucose control status.Key words: Glucose-6-PD; Diabetes; Female.DOI: 10.3329/jbsp.v5i2.6778J Bangladesh Soc Physiol. 2010 December; 5(2): 60-65

Hyperglycemia causes oxidative stress in pancreatic beta-cells of GK rats, a model of type 2 diabetes

Diabetes ◽  
1999 ◽  
Vol 48 (4) ◽  
pp. 927-932 ◽  
Author(s):  
Y. Ihara ◽  
S. Toyokuni ◽  
K. Uchida ◽  
H. Odaka ◽  
T. Tanaka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Gk Rats

Fasting Glucose-to-HbA1c Ratio Is a Good Indicator of G6PD Deficiency in Patients with Type 2 Diabetes

2019 ◽  
Author(s):  
Ya-Sian Chang ◽  
Li-Yun Hsiao ◽  
Chien-Yu Lin ◽  
Mu-Chin Shih ◽  
Ming-Chia Hsieh ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
G6pd Deficiency ◽  
Fasting Glucose

Alpha-1-Antichymotrypsin: a Common Player for Type 2 Diabetes and Alzheimer's Disease

2020 ◽  
Vol 16 ◽  
Author(s):  
Nataly Guzmán-Herrera ◽  
Viridiana C. Pérez-Nájera ◽  
Luis A. Salazar-Olivo
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Type 2 Diabetes ◽  
Alzheimer's Disease ◽  
Regulatory Networks ◽  
Therapeutic Strategies ◽  
Oxidative Stresses ◽  
Bibliographic Search ◽  
And Oxidative Stress

Background: Numerous studies have shown a significant association between type 2 diabetes mellitus (T2D) and Alzheimer's disease (AD), two pathologies affecting millions of people worldwide. Chronic inflammation and oxidative stress are two conditions common to these diseases also affecting the activity of the serpin alpha-1-antichymotrypsin (ACT), but a possible common role for this serpin in T2D and AD remains unclear. Objective: To explore the possible regulatory networks linking ACT to T2D and AD. Materials and Methods: A bibliographic search was carried out in PubMed, Med-line, Open-i, ScienceDirect, Scopus and SpringerLink for data indicating or suggesting association among T2D, AD, and ACT. Searched terms like “alpha-1-antichymotrypsin”, “type 2 diabetes”, “Alzheimer's disease”, “oxidative stress”, “pro-inflammatory mediators” among others were used. Moreover, common therapeutic strategies between T2D and AD as well as the use of ACT as a therapeutic target for both diseases were included. Results: ACT has been linked with development and maintenance of T2D and AD and studies suggest their participation through activation of inflammatory pathways and oxidative stress, mechanisms also associated with both diseases. Likewise, evidences indicate that diverse therapeutic approaches are common to both diseases. Conclusion: Inflammatory and oxidative stresses constitute a crossroad for T2D and AD where ACT could play an important role. In-depth research on ACT involvement in these two dysfunctions could generate new therapeutic strategies for T2D and AD.

scholarly journals Novel Soy Germ Pasta Improves Endothelial Function, Blood Pressure, and Oxidative Stress in Patients With Type 2 Diabetes: Figure 1

Diabetes Care ◽  
2011 ◽  
Vol 34 (9) ◽  
pp. 1946-1948 ◽  
Author(s):  
Carlo Clerici ◽  
Elisabetta Nardi ◽  
Pier Maria Battezzati ◽  
Stefania Asciutti ◽  
Danilo Castellani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Endothelial Function ◽  
And Oxidative Stress

scholarly journals MicroRNAs and Oxidative Stress: An Intriguing Crosstalk to Be Exploited in the Management of Type 2 Diabetes

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 802
Author(s):  
Teresa Vezza ◽  
Aranzazu M. de Marañón ◽  
Francisco Canet ◽  
Pedro Díaz-Pozo ◽  
Miguel Marti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Signaling Pathways ◽  
Current Knowledge ◽  
Critical Role ◽  
Cell Dysfunction ◽  
Non Coding Rnas ◽  
And Oxidative Stress ◽  
Molecular Crosstalk

Type 2 diabetes is a chronic disease widespread throughout the world, with significant human, social, and economic costs. Its multifactorial etiology leads to persistent hyperglycemia, impaired carbohydrate and fat metabolism, chronic inflammation, and defects in insulin secretion or insulin action, or both. Emerging evidence reveals that oxidative stress has a critical role in the development of type 2 diabetes. Overproduction of reactive oxygen species can promote an imbalance between the production and neutralization of antioxidant defence systems, thus favoring lipid accumulation, cellular stress, and the activation of cytosolic signaling pathways, and inducing β-cell dysfunction, insulin resistance, and tissue inflammation. Over the last few years, microRNAs (miRNAs) have attracted growing attention as important mediators of diverse aspects of oxidative stress. These small endogenous non-coding RNAs of 19–24 nucleotides act as negative regulators of gene expression, including the modulation of redox signaling pathways. The present review aims to provide an overview of the current knowledge concerning the molecular crosstalk that takes place between oxidative stress and microRNAs in the physiopathology of type 2 diabetes, with a special emphasis on its potential as a therapeutic target.

scholarly journals Synergistic Effects of Milk-Derived Exosomes and Galactose on α-Synuclein Pathology in Parkinson’s Disease and Type 2 Diabetes Mellitus

2021 ◽  
Vol 22 (3) ◽  
pp. 1059
Author(s):  
Bodo C. Melnik
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Dopaminergic Neurons ◽  
Vagal Nerve ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
The Brain

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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