Depletion of total antioxidant capacity in type 2 diabetes

Opara, Emmanuel C.; Abdelrahman, Eman; Soliman, Sohair; Kamel*, Wasan Munim Niran; Souka, Samia; Lowe, James E.; Abdel-aleem, Salah

doi:10.1016/s0026-0495(99)90152-x

Cited by 126 publications

(80 citation statements)

References 26 publications

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“…A decline in reduced glutathione, vitamin C, vitamin E, and lipoic acid is noted in patients with diabetes (Shigeta et al 1961, Maxwell et al 1997, Opara et al 1999. In vitro studies and studies in animal insulin resistance models have shown that antioxidants, especially a-lipoic acid, vitamin E, and vitamin C improve insulin sensitivity (Evans & Goldfine 2000, Jacob et al 2000.…”

Section: Introductionmentioning

confidence: 99%

Antioxidants preserve redox balance and inhibit c-Jun-N-terminal kinase pathway while improving insulin signaling in fat-fed rats: evidence for the role of oxidative stress on IRS-1 serine phosphorylation and insulin resistance

Vinayagamoorthi¹,

Bobby²,

Sridhar³

2008

Journal of Endocrinology

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The oxidative stress-sensitive c-Jun-N-terminal kinase (JNK) pathway is known to be activated in diabetic condition and is involved in the progression of insulin resistance. However, the effect of antioxidants on JNK pathway and insulin resistance has not been investigated. The present study was aimed to investigate the effect of antioxidants on redox balance, insulin sensitivity, and JNK pathway in high-fat-fed rats. Male Wistar rats were divided into four groups: the control group -received a rodent chow; controlCantioxidant group -fed with rodent chow supplemented with 0 . 2% (w/w) vitamin E, 0 . 3% (w/w) vitamin C, and 0 . 5% (w/w) a-lipoic acid; high-fat groupreceived high-fat diet; and high fatCantioxidant group -fed with high-fat diet supplemented with above antioxidants. Fat feeding to rats for 9 weeks significantly increased IRS-1 serine phoshorylation, reduced insulin-stimulated IRS-1 tyrosine phosphorylation and insulin sensitivity. High-fat diet also impaired redox balance and activated the redox-sensitive serine kinase -JNK pathway. Antioxidant supplementation along with high-fat diet preserved the free radical defense system, inhibited the activation of JNK pathway, and improved insulin signaling and insulin sensitivity. The present study shows for the first time that antioxidants inhibit JNK pathway and IRS-1 serine phosphorylation while improving insulin sensitivity in fat-fed rats. These findings implicate the beneficial effect of antioxidants in obesity-/dyslipidemia-induced insulin resistance in humans.

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Section: Introductionmentioning

confidence: 99%

Antioxidants preserve redox balance and inhibit c-Jun-N-terminal kinase pathway while improving insulin signaling in fat-fed rats: evidence for the role of oxidative stress on IRS-1 serine phosphorylation and insulin resistance

Vinayagamoorthi¹,

Bobby²,

Sridhar³

2008

Journal of Endocrinology

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“…In other experimental model of diabetes authors observed decreased levels of renal catalase despite of increased levels of heart catalase, kidney and heart SOD, and liver GPx [28]. T2DM patients, with or without proteinuria, a biomarker of renal damage, had very lower TAC levels compared with the control group (DM-free) (1.7 mmol/L and 1.4 mmol/L versus 2.7 mmol/L) [3]. In the same manner, it was verifyied a significant impairment of plasma TAC and GSH and an increase of lipid peroxidation in T1DM children patients [5].…”

Section: Is Diabetes Mellitus Associated With Decrease Total Antioxidmentioning

confidence: 95%

“…As a consequence of the oxidative and nitrosative stresses occurs lipid peroxidation (measured by biomarkers like malonaldehyde, 4-hydroxynonenal, and conjugated dienes), protein and aminoacid oxidation (evaluated by protein carbonyls), nucleic acid oxidation (quantifyied by DNA oxidized bases) and carbohydrate oxidation (measured by glycosilation products like glycated hemoglobin [HbA1] and advanced glycation end products [AGEs] commonly found in DM animal models and human patients [3][4][5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Antioxidant defenses in diabetes mellitus: a clinical and molecular approach

Ferrari¹

2017

Integr Obesity Diabetes

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Oxidative and nitrosative stress reactions are implicated in cell and organ damage due to diabetes mellitus. In both type 1 and type 2 DM there is a massive oxidative and nitrosative stresses which have been associated with intensive changes on both antioxidant enzyme systems (SOD, CAT, GPx, GSH) and total antioxidant capacity (TAC) causing peroxidative damage to lipids, proteins, nucleic acids and carbohydrates which can be used as DM biomarkers. Molecular pathophysiology of diabetes mellitus envolves induction of the the NFkB and p38-MAPK cell signaling pathways by Rac, TNF-α, TLR4, decrease of antioxidant defenses, and direct mitochondrial damage. Knowledge of molecular pathways is essential for research of newer preventive and therapeutic approaches in diabetes mellitus complications (atherosclerosis, myocardial damage, endothelial dysfunction, and renal failure).urine, feces, tissue sample), vegetable or fruit extract or even foods or pharmaceuticals [14][15][16].This article review and update the clinical, cellular, and molecular knowledge of free radicals and antioxidant defenses in diabetes mellitus. Ethiopathogenesis of diabetes mellitus I and IIDiabetes mellitus has been conceptualized as a group of metabolic disorders characterized by hyperglicemia as a result of insulin secretion failure and/or lacking of insulin action on target cells. The chronic diabetic hyperglicemic state has been related to long-term organ damage especially to the heart, endothelium and blood vessels, nerves, kidney, and eyes [17][18][19].

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“…A study conducted in Egyptian population reported that depletion of the TAS is associated with diabetic complications [30]. Furthermore, another study has reported a significant decrease in TAS in patients with diabetic neuropathy [31].…”

Section: Association Between Tas and Type 2 Diabetes Mellitusmentioning

confidence: 99%

Assessment of Dna Strand Breaks and Total Antioxidant Status in Type 2 Diabetic Patients With and Without Complications- A Case-Control Study

Nithya

Isabel²,

Angeline³

et al. 2017

Asian J Pharm Clin Res

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Objective: To evaluate the total antioxidant status (TAS) and the extent of DNA strand breaks (damage) as a measure of oxidative stress biomarkers in patients with Type 2 diabetes (with and without complications) and controls.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). TAS was assessed by ferric reducing ability of plasma assay.Results: TAS was found to be significantly lower in patients with Type 2 diabetes (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 patients with diabetes (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 hemoglobin level (HbA 1C ) were found to be significantly higher in patients with diabetes than controls (p<0.05). Correlation analysis showed that there is no association between age, duration, sugar level, HbA 1C , TAS, and DNA damage in patients with Type 2 diabetes mellitus. Conclusion:Alterations in TAS and the extent of DNA damage were 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.

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Depletion of total antioxidant capacity in type 2 diabetes

Cited by 126 publications

References 26 publications

Antioxidants preserve redox balance and inhibit c-Jun-N-terminal kinase pathway while improving insulin signaling in fat-fed rats: evidence for the role of oxidative stress on IRS-1 serine phosphorylation and insulin resistance

Antioxidants preserve redox balance and inhibit c-Jun-N-terminal kinase pathway while improving insulin signaling in fat-fed rats: evidence for the role of oxidative stress on IRS-1 serine phosphorylation and insulin resistance

Antioxidant defenses in diabetes mellitus: a clinical and molecular approach

Assessment of Dna Strand Breaks and Total Antioxidant Status in Type 2 Diabetic Patients With and Without Complications- A Case-Control Study

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