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A Systematic Review of Oxidative Stress and Safety of Antioxidants in Diabetes: Focus on Islets and Their Defense
Udayakumar Karunakaran, Keun-Gyu Park
Diabetes Metab J. 2013;37(2):106-112.   Published online April 16, 2013
DOI: https://doi.org/10.4093/dmj.2013.37.2.106
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AbstractAbstract PDFPubReader   

A growing body of evidence suggests that hyperglycemia-induced oxidative stress plays an important role in diabetic complications, especially β-cell dysfunction and failure. Under physiological conditions, reactive oxygen species serve as second messengers that facilitate signal transduction and gene expression in pancreatic β-cells. However, under pathological conditions, an imbalance in redox homeostasis leads to aberrant tissue damage and β-cell death due to a lack of antioxidant defense systems. Taking into account the vulnerability of islets to oxidative damage, induction of endogenous antioxidant enzymes or exogenous antioxidant administration has been proposed as a way to protect β-cells against diabetic insults. Here, we consider recent insights into how the redox response becomes deregulated under diabetic conditions, as well as the therapeutic benefits of antioxidants, which may provide clues for developing strategies aimed at the treatment or prevention of diabetes associated with β-cell failure.

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Original Articles
The Relationship between Apolipoprotein E Phenotypes, Serum Lipid Metabolism, and Oxidative Stress in Korean Type 2 Diabetic Patients.
Soo Bong Choi, Sun Min Park
Korean Diabetes J. 1999;23(2):182-192.   Published online January 1, 2001
  • 1,015 View
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AbstractAbstract PDF
BACKGROUND
The cause of type 2 diabetes mellitus (DM) is not known, but one of the causes may be the reduction of insulin secretion through the fibrosis formed with amyloid deposits in pancreatic beta cells. Amyloidogenesis in hippocampus is a characteristic feature in Alzheimers disease. Possession of the Apolipoprotein (Apo) E 4 allele (E4/2, FA/3 or E4/4) is a risk factor for the development of Alzheimers disease. However, it is controversial that Apo E polymophsim is associated with the etiopathology of type 2 DM. Both Alzheimers disease and type 2 DM has increased oxidative stress, which may be related to the formation of fibrosis. The purpose of this study was to investigate the distribution of Apo E phenotypes in type 2 diabetic subjects and healthy subjects, and to determine whether Apo E phenotypes influenced serum lipid profiles and glutathione peroxidase and superoxide dismutase activities of red blood cells in type 2 DM and healthy subjects. METHODS: Overnight fasting blood was collected from 84 type 2 diabetic patients and 85 healthy subjects. Apo E phenotypes was determined by the isoelectrofocusing method. Serum lipid profiles and supetoxide dismutase and glutathione peroxidase activ'ities of red blood cells (RBC) were measured. RESULTS: The frequency of Apo E 4 in the type 2 DM was higher than that in the control group (p<0,05). The serum total cholesterol and triglyceride levels of the type 2 DM were overall higher than in healthy subjects. Serum lipid profiles were not affected by Apo E phenotypes in healthy subjects. However, semm total cholesterol levels of type 2 diab diabetic patients with Apo E3/3 were signifcantly lower than those with Apo FA/3 (p<0.05), but serum HDL, cholesterol levels had an opposite tendency. Serum triglyceride levels of type 2 diabetic patients with Apo E3/2 were higher than those with Apo E4/3 (p<0.05), RBC superoxide dismutase and gluta,thione peroxidase activities in type 2 diabetic patients tended to be lower than those in the control group. These enzyme activities of type 2 diabetic patieints with Apo E3 were lowest among the Apo E phenotype groups (p<0.05). CONCLUSION: This result suggests that type 2 diabctic patients had more Apo E 4 allele than in healthy people. Antioxidant enzyme activities decrqased in type 2 diabetic patients with Apo E 4 allele. Serum lipid profiles of type 2 diabetic patients with Apo E 4 allele was an increased risk factor for cardiovascular disease.
The Effect of High Glucose on the Activity of Superoxide Dismutase in NIN6N8a Cells.
Hak Yeon Bae, Byoung Rai Lee, Kwang Sam Kho
Korean Diabetes J. 1998;22(3):271-289.   Published online January 1, 2001
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  • 18 Download
AbstractAbstract PDF
BACKGROUND
Reactive oxygen species play a role in the pathogenesis of diabetes mellitus. Hyperglycemia may cause increased production of free radicals, and peroxide formation was increased in high glucose solution. It has been demonstrated that active oxygen species induce antioxidant enzyme expression in some tissues and cells. This study was designed to investigate the effect of high glucose on the activity of superoxide dismutase(SOD) in mouse insulinoma(MIN6N8a) cells. METHODS: MIN6N8a cells were grown in RPMI1640 medium with l0% fetal bovine serum and NIH3T3 cells used as a control cells. The cells were cultured in 5.6 and 22.2 mM glucose cnntained medium. The activities of SOD, catalase and GPX were determined in crude cell extract after 7 days of culture. The levels of CuZn-SOD were also measured with ELISA using anti-CuZn-SOD antibody. RESULTS: In MIN6NSa cells, the catalase activity was very low compared with NIH3T3 cells, but there was no difference in activities of CuZn-SOD and GPX between MIN6N8a cells and NIH3T3 cells. The activity of CuZn-SOD was decreased, while Mn-SOD was increased in MIN6NSa cells cultured with high glucose(22.2 mM) medium compared with those of normoglucose(5.6 mM) medium. However, the level of CuZn-SOD in MIN6NSa cells, when measured with ELISA was high in cells of cultured with high glucose medium. The SOD activity was not effected in MIN6N8a cells cultured with insulin contained medium. CONCLUSION: These experimental result suggest that the CuZn-SOD activity was decreased in MIN6N8a cells cultured with high glucose contained medium and this effect may be resulted from the protein inactivation rather than decrement of protein level.

Diabetes Metab J : Diabetes & Metabolism Journal
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