Decreased total antioxidant levels and increased oxidative stress in South African type 2 diabetes mellitus patients

Abstract This work aims to examine the interaction between Apolipoprotein A2 (Apo A-II) −265T>C single nucleotide polymorphism (SNP) and dietary total antioxidant capacity (DTAC) on inflammation and oxidative stress in patients with type 2 diabetes mellitus. The present cross-sectional study included 180 patients (35-65 years) with identified Apo A-II genotype. Dietary intakes were assessed by a food frequency questionnaire. DTAC was computed using the international databases. Interleukin-18(IL18), high-sensitivity C-reactive protein (hs-CRP), and pentraxin (PTX3), serum total antioxidant capacity (TAC), superoxide dismutase activity (SOD), and 8-isoprostaneF2α (PGF2α) markers were obtained according to standard protocols. General linear model was used to evaluate the interaction. The interaction of gene and DTAC (PFRAP=0.039 and PORAC=0.042) on PGF2α level was significant after adjusting for confounders. A significant interaction was observed on IL18 level (PORAC=0.018 and PFRAP=0.048) and SOD (PTEAC=0.037) in obese patients. Among patients whose DTAC was higher than the median intake, the levels of hs-CRP and PGF2α were significantly higher only in individuals with CC genotype. Serum TAC (PFRAP=0.030, PORAC=0.049) and SOD were significantly lower in the CC genotype. There was a favorable relationship between the high-DTAC and SOD (Obese: PTEAC=0.034, Non-obese: PFRAP=0.001, PTRAP<0.0001, PTEAC=0.003 and PORAC=0.001) and PGF2α (Non-obese: PORAC=0.024) in T-allele carriers. The rs5082 SNP interacts with DTAC to influence several cardio-metabolic risk factors. Also, we found dietary recommendations for antioxidant-rich foods intake might be useful in the prevention of diabetes complications in the T carrier more effectively than the CC genotype. Future large studies are required to confirm these results.

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Serum Lipoprotein (a) Levels in Black South African Type 2 Diabetes Mellitus Patients

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/5743838 ◽

2016 ◽

Vol 2016 ◽

pp. 1-5

Author(s):

Jim Joseph ◽

Farzana Ganjifrockwala ◽

Grace George

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Antioxidant Capacity ◽

South African ◽

Total Antioxidant Capacity ◽

Lipoprotein A ◽

Black South African ◽

Total Antioxidant

Lipoprotein (a) (Lp(a)) which is a low-density lipoprotein-like particle containing apo(a) is considered as an emergent cardiovascular risk factor. Type 2 diabetes mellitus (T2DM) is associated with a two- to threefold increase in the risk of cardiovascular disease (CVD). The aim of this study was to investigate the levels of Lp(a) in Black South African T2DM patients and its association with other metabolic factors. 67 T2DM patients and 48 healthy control participants were recruited for the cross-sectional study. The Lp(a) level was determined by ELISA and the result was analyzed using SPSS. The Lp(a) level in diabetics was found to be significantly increased (P=0.001) when compared to the normal healthy group. In the diabetic group, the Lp(a) levels correlated significantly with the duration of diabetes (P=0.008) and oxidized LDL (ox-LDL) levels (P=0.03) and decreased total antioxidant capacity (P=0.001). The third tertile of Lp(a) was significantly correlated with increased ox-LDL, C-reactive protein, and triglycerides and decreased total antioxidant capacity.

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ASSESSMENT OF DNA STRAND BREAKS AND TOTAL ANTIOXIDANT STATUS IN TYPE 2 DIABETIC PATIENTS WITH AND WITHOUT COMPLICATIONS- A CASE-CONTROL STUDY

Asian Journal of Pharmaceutical and Clinical Research ◽

10.22159/ajpcr.2017.v10i4.17020 ◽

2017 ◽

Vol 10 (4) ◽

pp. 430

Author(s):

K Nithya ◽

Isabel W ◽

Angeline T ◽

Priscilla As ◽

Asirvatham Aj

Keyword(s):

Oxidative Stress ◽

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Dna Damage ◽

Type 2 Diabetes Mellitus ◽

Antioxidant Status ◽

Total Antioxidant Status ◽

Diabetic Patients ◽

Total Antioxidant

Objective: To evaluate the total antioxidant status (TAS) and the extent of DNA strand breaks (damage) as a measure of oxidative stress biomarkers in Type 2 diabetic patients (with and without complications) and controls.Materials and Methods: Blood samples were collected from 200 patients with type 2 diabetes mellitus (n=100 with complications and n=100 without complications) and 100 healthy individuals. Oxidative DNA damage was evaluated using alkaline single cell gel electrophoresis (comet assay). Total antioxidant status was assessed by Ferric Reducing Ability of Plasma (FRAP) assay.Results: TAS was found to be significantly lower in type 2 diabetic patients (with and without complications) compared to controls (p< 0.001). Similarly, patients with complications of type 2 diabetes mellitus had significantly lower TAS when compared to diabetic patients (p= 0.007). DNA damage analysis showed that the extent of damage was high in patients with diabetes mellitus (with and without complications) compared to controls (p< 0.001). Fasting glucose and glycosylated haemoglobin level (HbA1c) was found to be significantly higherin diabetic patients than controls (p< 0.05). Correlation analysis showed that there is no association between age, duration, sugar level, HbA1c, TAS and DNA damage in patients with Type 2 diabetes mellitus.Conclusion: Alterations in TAS and the extent of DNA damage was observed in patients with complications of diabetes mellitus indicate that oxidative stress is more in patients with complications when compared to patients without complications and healthy individuals. Therefore, further DNA damage and onset of complications in Type 2 diabetes mellitus could be prevented by counteracting the oxidative stress by therapeutic interventions using appropriate antioxidants.Key words: Hyperglycemia, Oxidative stress, DNA damage, Total antioxidant status, Type 2 diabetes mellitus, Vascular complication

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Rubusoside Reduces Blood Glucose and Inhibits Oxidative Stress by Activating the AMPK Signaling Pathway in Type 2 Diabetes Mellitus Mice

Natural Product Communications ◽

10.1177/1934578x211069230 ◽

2022 ◽

Vol 17 (1) ◽

pp. 1934578X2110692

Author(s):

Xi-yu Hu ◽

Ying Chang ◽

Zheng-zhe Xu ◽

Yan Wang ◽

Min-min Dai ◽

...

Keyword(s):

Oxidative Stress ◽

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Body Weight ◽

Blood Glucose ◽

Total Antioxidant Capacity ◽

Candidate Drug ◽

Total Antioxidant

The current study aimed at investigating the therapeutic effects of rubusoside on type 2 diabetes mellitus (T2DM) mice models as an alternative hypoglycemic candidate drug. T2DM mice models were established with a combination of streptozotocin (STZ) intraperitoneal injection and high-fat diet. After 10 weeks of rubusoside intragastric administration (100, 200 mg/kg/day) to the mice, the body weight, fasting blood glucose, glucose tolerance, and blood lipids were measured. The liver protein expression levels of p-AMPK, GLUT2, GLUT4 and total antioxidant capacity were also investigated. After 10 weeks of rubusoside administration, the levels of blood glucose and lipids were decreased in T2DM mice. Compared with the model group, rubusoside administration significantly decreased the liver mass-to-body weight ratio, upregulated p-AMPK and GLUT4, and downregulated GLUT2 expression levels in the liver. Activities of superoxide dismutase (SOD), catalase (CAT), and gluathione peroxidase (GSH-Px) were increased, and the concentration of malondialdehyde (MDA) was decreased to reduce oxidative stress in the liver. Liver hematoxylin and eosin (H&E) pathological analysis also showed that rubusoside had a protective effect on T2DM mice liver. These results demonstrate that rubusoside could be used as an anti-diabetic candidate drug, and that its hypoglycemic mechanism might be related to the activation of adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) to modulate the expression of GLUT2 and GLUT4. Finally, rubusoside could also increase total antioxidant capacity to protect the liver from oxidative stress.

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910-P: Relationship between Continuous Glucose Monitoring Metrics and Oxidative Stress in Patients with Type 2 Diabetes Mellitus: A Cross-Sectional Study

Diabetes ◽

10.2337/db20-910-p ◽

2020 ◽

Vol 69 (Supplement 1) ◽

pp. 910-P

Author(s):

YO KOHATA ◽

MAKOTO OHARA ◽

TOMOKI FUJIKAWA ◽

HIROE NAGAIKE ◽

HIDEKI KUSHIMA ◽

...

Keyword(s):

Oxidative Stress ◽

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Glucose Monitoring ◽

Cross Sectional Study ◽

Sectional Study ◽

Cross Sectional ◽

And Oxidative Stress

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

International Journal of Molecular Sciences ◽

10.3390/ijms22031059 ◽

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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