Oxidative Stress-Related Genes in Type 2 Diabetes: Association Analysis and Their Clinical Impact

Haldar, Suranjana Ray; Chakrabarty, Arpita; Chowdhury, Subhankar; Haldar, Atish; Sengupta, Sanghamitra; Bhattacharyya, Maitree

doi:10.1007/s10528-015-9675-z

Cited by 33 publications

(18 citation statements)

References 40 publications

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“…Data presented here show that the Turkish population has the similar GG genotype frequency as seen in Chinese [3], Iranian [33], and Polish populations [15]. We detected higher GG genotype frequency than those found in American populations [6] and fairly lower frequencies than those found in Chinese [4,17], Korean [32], Indian [35], Iranian [34] populations. Eventually, GG genotype frequency in populations of the eastern countries have been found higher (between 0.3 and 34.8%) than the western countries (between 0.0 and 0.82%) ( Table 3).…”

Section: Discussionsupporting

confidence: 71%

Superoxide Dismutase 1 (SOD 1) A251G Polymorphism

Siliğ

Taş

Şahin‐Bölükbaşı

et al. 2017

Turkish Journal of Biochemistry

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Objective: A genetic polymorphism of SOD1 A251G(rs2070424) is in the 3rd intron region of the SOD gene. The aim of this study was to determine the frequencies of the polymorphisms of the SOD1 A251G in a Turkish population, including 494 healthy individuals. Methods: The 494 Turkish individuals were genotyped for polymorphisms of SOD1 gene. The distribution of SOD1 A251G polymorphisms in this population was examined using a PCR-RFLP method. Genotype and allele frequencies were estimated by counting. Hardy-Weinberg equation between expected and observed genotype distributions was assessed using the X 2 test. Results: In the present study, the distribution of SOD1 A251G polymorphisms in a Turkish population including 494 (females: 278, 56.3% and males: 216, 43.7%) healthy individuals was examined. The mean age of the study population was 38.4 ± 16.6 years (males, 39.8 ± 17.1; females, 37.3 ± 16.1). The observed genotype frequencies of SOD1 A251G were 86.2, 13.4 and 0.4% for AA, AG and GG, respectively. Conclusions: This study provides basic information about the allele and genotype frequency distributions of polymorphisms in the SOD1 A251G gene studied. These frequencies may be useful parameters as a reference for future studies on genetic basis of various diseases and cancer susceptibility. Özet Amaç: SOD1 A251G (rs2070424) genetik polimorfizmi SOD geninin 3. intron bölgesinde lokalizedir. Bu çalışma 494 sağlıklı birey içeren bir Türk popülasyonunda SOD1 A251G polimorfiziminin frekanslarını belirlemeyi amaçlamıştır. Yöntemler: Bu çalışmada, 494 sağlıklı Türk bireyin SOD1 geninin polimorfizmi genotiplendi. Bu popülasyonda SOD1 A251G polimorfizmin dağılımı bir PCR-RFLP yöntemi kullanılarak incelenmiştir. Genotip ve alel frekansları sayarak elde edilmiştir. Beklenen ve gözlenen genotip dağılımları arasında Hardy-Weinberg dengesi X 2 testi kullanılarak değerlendirilmiştir. Bulgular: Bu çalışmada, SOD1 genindeki A251G polimorfizmi toplam 494 (females: 278, 56.3% and males: 216, 43.7%) Türk sağlıklı birey incelendi. Çalışma grubunun yaş ortalaması 38.4 ± 16.6 yıl (erkek, 39.8 ± 17.1; kadın, 37.3 ± 16.1) idi. SOD1 gözlenen genotip frekansları sıra-sıyla AA: % 86.2 AG: % 13.4 ve GG için % 0.4 olarak tespit edildi. Sonuç: Bu çalışma, Türk toplumunda SOD1 A251G gen polimorfizmlerinin alel ve genotip frekans dağılımları hakkında temel bilgiler sağlamıştır. Türk popülasyo-nunda SOD1 A251G polimorfizmi ile yapılan ilk çalışmadır ve önemlidir. Bu frekanslar gelecekte çeşitli hastalıklar ve kanser yatkınlığı çalışmalarında yararlı referans parametreler olabilir.

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Section: Discussionsupporting

confidence: 71%

Superoxide Dismutase 1 (SOD 1) A251G Polymorphism

Siliğ

Taş

Şahin‐Bölükbaşı

et al. 2017

Turkish Journal of Biochemistry

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“…Oxidative stress has been thought to play a central role in the pathogenesis of diabetes and its complications [160][161][162][163][164][165][166]. It is induced by overwhelming production of ROS that can attack macromolecules including lipids, DNA, and proteins [28, [167][168][169][170].…”

Section: Oxidative Stressmentioning

confidence: 99%

Hyperglycemic Stress and Carbon Stress in Diabetic Glucotoxicity

Luo¹,

Wu²,

Si-qun³

et al. 2016

Aging and disease

111

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Diabetes and its complications are caused by chronic glucotoxicity driven by persistent hyperglycemia. In this article, we review the mechanisms of diabetic glucotoxicity by focusing mainly on hyperglycemic stress and carbon stress. Mechanisms of hyperglycemic stress include reductive stress or pseudohypoxic stress caused by redox imbalance between NADH and NAD + driven by activation of both the polyol pathway and poly ADP ribose polymerase; the hexosamine pathway; the advanced glycation end products pathway; the protein kinase C activation pathway; and the enediol formation pathway. Mechanisms of carbon stress include excess production of acetyl-CoA that can over-acetylate a proteome and excess production of fumarate that can over-succinate a proteome; both of which can increase glucotoxicity in diabetes. For hyperglycemia stress, we also discuss the possible role of mitochondrial complex I in diabetes as this complex, in charge of NAD + regeneration, can make more reactive oxygen species (ROS) in the presence of excess NADH. For carbon stress, we also discuss the role of sirtuins in diabetes as they are deacetylases that can reverse protein acetylation thereby attenuating diabetic glucotoxicity and improving glucose metabolism. It is our belief that targeting some of the stress pathways discussed in this article may provide new therapeutic strategies for treatment of diabetes and its complications.

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“…Several genetic polymorphisms in oxidative stress pathways have recently been linked to the complications of DM (81). Agents that can promote the complications of DM, such as advanced glycation end products (AGEs) (30), result in the release of ROS, caspase activation (47, 82-84), and loss of anti-oxidant levels (85).…”

Section: Cellular Injury With Diabetes Mellitusmentioning

confidence: 99%

FoxO Transcription Factors and Regenerative Pathways in Diabetes Mellitus

Maiese¹

2015

CNR

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Mammalian forkhead transcription factors of the O class (FoxO) are exciting targets under consideration for the development of new clinical entities to treat metabolic disorders and diabetes mellitus (DM). DM, a disorder that currently affects greater than 350 million individuals globally, can become a devastating disease that leads to cellular injury through oxidative stress pathways and affects multiple systems of the body. FoxO proteins can regulate insulin signaling, gluconeogenesis, insulin resistance, immune cell migration, and cell senescence. FoxO proteins also control cell fate through oxidative stress and pathways of autophagy and apoptosis that either lead to tissue regeneration or cell demise. Furthermore, FoxO signaling can be dependent upon signal transduction pathways that include silent mating type information regulation 2 homolog 1 (S. cerevisiae) (SIRT1), Wnt, and Wnt1 inducible signaling pathway protein 1 (WISP1). Cellular metabolic pathways driven by FoxO proteins are complex, can lead to variable clinical outcomes, and require in-depth analysis of the epigenetic and post-translation protein modifications that drive FoxO protein activation and degradation.

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Oxidative Stress-Related Genes in Type 2 Diabetes: Association Analysis and Their Clinical Impact

Cited by 33 publications

References 40 publications

Superoxide Dismutase 1 (SOD 1) A251G Polymorphism

Superoxide Dismutase 1 (SOD 1) A251G Polymorphism

Hyperglycemic Stress and Carbon Stress in Diabetic Glucotoxicity

FoxO Transcription Factors and Regenerative Pathways in Diabetes Mellitus

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