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Hyperglycemia, Oxidative Stress, and Identification of Oxidative Stress Parameters in Type 2 Diabetes

Yıl 2020, Cilt: 4 Sayı: 1, 60 - 68, 23.04.2020
https://doi.org/10.25048/tudod.638744

Öz

Oxidative stress is an important actor that can play a role in both the development of Type 2 diabetes and the development of diabetes complications. Basically, oxidative stress is used to describe the physiological state resulting from the disruption of the balance between the production and degradation of reactive oxygen derivatives (ROS). Data obtained from clinical studies show that systemic oxidative stress is closely related to metabolic syndrome and its components. Chronic hyperglycemia and hyperlipidemia are important risk factor for ROS formation. The contribution of hyperglycemia to ROS accumulation can occur through different metabolic pathways. Increased activity of the glycolytic pathway under hyperglycemic conditions and electron pressure on the mitochondrial electron transport system contribute to ROS formation. The formation and accumulation of reactive oxygen derivatives forces the cell to metabolize glucose with alternative pathways by suppressing the activity of glyceraldehyde 3-P dehydrogenase (GAPDH) enzyme which is one of the key enzymes involved in glycolysis. While the effectiveness of the glycolysis and krebs cycle decreases, polyol pathway, hexosamine pathway and Protein Kinase C (PCK) activity increase. All of these alternative metabolic pathways further increase ROS formation in the cell. ROS accumulation may contribute to the pathogenesis of insulin resistance by reducing the gene expression of insulin and the release of insulin from beta cells via posttranslational factors. ROS accumulation due to hyperglycemia also plays an important role in the development of diabetes complications. The results of clinical studies indicate that many markers can be used to determine the oxidative damage caused by diabetes and its complications in the protein, lipid and nucleic acid components of the cell and these markers may also give an idea about the level of oxidant damage

Kaynakça

  • 1. Robertson RP. Chronic oxidative stress as a central mechanism for glucose toxicity in pancreatic islet beta cells in diabetes. J Biol Chem. 2004;279(41):42351–4.
  • 2. Wright E, Scism-Bacon JL, Glass LC, Glass L. Oxidative stress in type 2 diabetes: the role of fasting and postprandial glycaemia. Int J Clin Pract. 2006;60(3):308–14.
  • 3. Yan L-J. Pathogenesis of chronic hyperglycemia: from reductive stress to oxidative stress. J Diabetes Res. 2014;2014:137919.
  • 4. Lorenzi M. The polyol pathway as a mechanism for diabetic retinopathy: attractive, elusive, and resilient. Exp Diabetes Res. 2007;2007:61038.
  • 5. Tang WH, Martin KA, Hwa J. Aldose Reductase, Oxidative Stress, and Diabetic Mellitus. Front Pharmacol. 2012;3:87.
  • 6. Lee AY, Chung SS. Contributions of polyol pathway to oxidative stress in diabetic cataract. FASEB J. 1999;13(1):23–30.
  • 7. Drel VR, Pacher P, Ali TK, Shin J, Julius U, El-Remessy AB, et al. Aldose reductase inhibitor fidarestat counteracts diabetes-associated cataract formation, retinal oxidative-nitrosative stress, glial activation, and apoptosis. Int J Mol Med. 2008;21(6):667–76.
  • 8. Giacco F, Brownlee M. Oxidative stress and diabetic complications. Circ Res. 2010;107(9):1058–70.
  • 9. Ramirez MA, Borja NL. Epalrestat: An Aldose Reductase Inhibitor for the Treatment of Diabetic Neuropathy. Pharmacotherapy. 2008;28(5):646–55.
  • 10. Giannoukakis N. Drug evaluation: ranirestat--an aldose reductase inhibitor for the potential treatment of diabetic complications. Curr Opin Investig Drugs. 2006;7(10):916–23.
  • 11. Johnson BF, Nesto RW, Pfeifer MA, Slater WR, Vinik AI, Chyun DA, et al. Cardiac abnormalities in diabetic patients with neuropathy: effects of aldose reductase inhibitor administration. Diabetes Care. 2004;27(2):448–54.
  • 12. Schleicher ED, Weigert C. Role of the hexosamine biosynthetic pathway in diabetic nephropathy. Kidney Int. 2000;58(77):13–8.
  • 13. Pantaleon M, Tan HY, Kafer GR, Kaye PL. Toxic effects of hyperglycemia are mediated by the hexosamine signaling pathway and o-linked glycosylation in early mouse embryos. Biol Reprod. 2010;82(4):751–8.
  • 14. Semba RD, Huang H, Lutty GA, Van Eyk JE, Hart GW. The role of O-GlcNAc signaling in the pathogenesis of diabetic retinopathy. Proteomics Clin Appl. 2014;8(3–4):218–31.
  • 15. Horal M, Zhang Z, Stanton R, Virkamäki A, Loeken MR. Activation of the hexosamine pathway causes oxidative stress and abnormal embryo gene expression: Involvement in diabetic teratogenesis. Birth Defects Res Part A - Clin Mol Teratol. 2004;70(8):519–27.
  • 16. Yang X, Ongusaha PP, Miles PD, Havstad JC, Zhang F, So WV, et al. Phosphoinositide signalling links O-GlcNAc transferase to insulin resistance. Nature. 2008;451(7181):964–9.
  • 17. Cooksey RC, Hebert LF, Zhu J-H, Wofford P, Garvey WT, McClain DA. Mechanism of Hexosamine-Induced Insulin Resistance in Transgenic Mice Overexpressing Glutamine:Fructose-6-Phosphate Amidotransferase: Decreased Glucose Transporter GLUT4 Translocation and Reversal by Treatment with Thiazolidinedione 1. Endocrinology. 1999;140(3):1151–7.
  • 18. Soetikno V, Watanabe K, Lakshamanan AP, Arumugam S, Sari FR, Sukumaran V, et al. Role of Protein Kinase C-MAPK, Oxidative Stress and Inflammation Pathways in Diabetic Nephropathy. J Nephrol Ther. 2012;s2(1).
  • 19. Geraldes P, King GL. Activation of Protein Kinase C Isoforms and Its Impact on Diabetic Complications. Circ Res. 2010;106:1319–31.
  • 20. Luo X, Wu J, Jing S, Yan L-J. Hyperglycemic Stress and Carbon Stress in Diabetic Glucotoxicity. Aging Dis. 2016;7(1):90–110.
  • 21. Khaled A. Ahmed Ikram S. SM. Type 2 Diabetes and Vascular Complications: A pathophysiologic view. Biomed Res. 2010;21(2):147–15.
  • 22. Lind M, Odén A, Fahlén M, Eliasson B. The true value of HbA1c as a predictor of diabetic complications: simulations of HbA1c variables. PLoS One. 2009;4(2):e4412.
  • 23. Nagai R, Murray DB, Metz TO, Baynes JW. Chelation: a fundamental mechanism of action of AGE inhibitors, AGE breakers, and other inhibitors of diabetes complications. Diabetes. 2012;61(3):549–59.
  • 24. Kaneto H, Matsuoka T, Katakami N, Kawamori D, Miyatsuka T, Yoshiuchi K, et al. Oxidative stress and the JNK pathway are involved in the development of type 1 and type 2 diabetes. Curr Mol Med. 2007;7(7):674–86.
  • 25. Tabak O, Gelisgen R, Erman H, Erdenen F, Muderrisoglu C, Aral H, et al. Oxidative lipid, protein, and DNA damage as oxidative stress markers in vascular complications of diabetes mellitus. Clin Invest Med. 2011;34(3):E163–71.
  • 26. Dhanasekaran DN, Reddy EP. JNK signaling in apoptosis. Oncogene. 2008;27(48):6245–51.
  • 27. Grankvist K, Marklund SL, Taljedal I-B. CuZn-superoxide dismutase, Mn-superoxide dismutase, catalase and glutathione peroxidase in pancreatic islets and other tissues in the mouse. Biochem J. 1981;199:393–8.
  • 28. Eriksson JW. Metabolic stress in insulin’s target cells leads to ROS accumulation - A hypothetical common pathway causing insulin resistance. FEBS Lett. 2007;581(19):3734–42.
  • 29. Draznin B. Molecular mechanisms of insulin resistance: Serine phosphorylation of insulin receptor substrate-1 and increased expression of p85 α: The two sides of a coin. Diabetes. 2006;55(8):2392–7.
  • 30. Rains JL, Jain SK. Oxidative stress, insulin signaling, and diabetes. Free Radic Biol Med. 2011;50(5):567–75.
  • 31. Bouzakri K, Karlsson HKR, Vestergaard H, Madsbad S, Christiansen E, Zierath JR. IRS-1 serine phosphorylation and insulin resistance in skeletal muscle from pancreas transplant recipients. Diabetes. 2006;55(3):785–91.
  • 32. Bloch-Damti A, Bashan N. Proposed Mechanisms for the Induction of Insulin Resistance by Oxidative Stress. Antioxid Redox Signal. 2005;7(11–12):1553–67.
  • 33. Yang H, Jin X, Kei Lam CW, Yan SK. Oxidative stress and diabetes mellitus. Clin Chem Lab Med. 2011;49(11):1773–82.
  • 34. Safi SZ, Qvist R, Kumar S, Batumalaie K, Ismail IS Bin. Molecular mechanisms of diabetic retinopathy, general preventive strategies, and novel therapeutic targets. Biomed Res Int. 2014;2014:801269.
  • 35. Preedy VR. Aging: Oxidative Stress and Dietary Antioxidants. Aging: Oxidative Stress and Dietary Antioxidants. 2014. 3-13 p.
  • 36. Valavanidis A, Vlachogianni T, Fiotakis C. 8-Hydroxy-2′ -deoxyguanosine (8-OHdG): A critical biomarker of oxidative stress and carcinogenesis. J Environ Sci Heal - Part C Environ Carcinog Ecotoxicol Rev. 2009;27(2):120–39.
  • 37. Martín-Gallán P, Carrascosa A, Gussinyé M, Domínguez C. Biomarkers of diabetes-associated oxidative stress and antioxidant status in young diabetic patients with or without subclinical complications. Free Radic Biol Med. 2003;34(12):1563–74.
  • 38. Bloomer RJ, Fisher-Wellman KH. Blood oxidative stress biomarkers: influence of sex, exercise training status, and dietary intake. Gend Med. 2008;5(3):218–28. 39. Il’yasova D, Scarbrough P, Spasojevic I. Urinary biomarkers of oxidative status. Clin Chim Acta. 2012;413(19–20):1446–53.
  • 40. Frijhoff J, Winyard PG, Zarkovic N, Davies SS, Stocker R, Cheng D, et al. Clinical Relevance of Biomarkers of Oxidative Stress. Antioxid Redox Signal. 2015;23(14):1144–70.
  • 41. Zujko ME., Witkowska AM., Górska M., Wilk J., Kretowski A. Reduced intake of dietary antioxidants can impair antioxidant status in type 2 diabetes patients. Pol Arch Med Wewn. 2014;124(11):599–607.
  • 42. Zhang Y, Du Y, He J-F, Li K-J. 8-iso-prostaglandin-F2α: a possible trigger or accelerator of diabetic retinopathy. Int J Ophthalmol. 2016;9(1):163–5.
  • 43. Pandey KB, Mishra N, Rizvi SI. Protein oxidation biomarkers in plasma of type 2 diabetic patients. Clin Biochem. 2010;43(4–5):508–11.
  • 44. Chao M-R, Rossner P, Haghdoost S, Jeng HA, Hu C-W, Hu C-W. Nucleic acid oxidation in human health and disease. Oxid Med Cell Longev. 2013;2013:368651.
  • 45. Liu X, Gan W, Zou Y, Yang B, Su Z, Deng J, et al. Elevated Levels of Urinary Markers of Oxidative DNA and RNA Damage in Type 2 Diabetes with Complications. 2016;2016.
  • 46. Pan H, Zhang L, Guo M, Sui H, Li H, Wu W, et al. The oxidative stress status in diabetes mellitus and diabetic nephropathy. Acta Diabetol. 2010;47(S1):71–6.

Hiperglisemi, Oksidatif Stres ve Tip 2 Diyabette Oksidatif Stres Belirteçlerinin Tanımlanması

Yıl 2020, Cilt: 4 Sayı: 1, 60 - 68, 23.04.2020
https://doi.org/10.25048/tudod.638744

Öz

Oksidatif stres, hem Tip 2 diyabet oluşumu hem de diyabet komplikasyonlarının gelişiminde rol oynayabilen önemli bir aktördür. Temel olarak oksidatif stres, reaktif oksijen türevlerinin (ROS) yapımı ve bozunumu arasındaki dengenin bozulması sonucunda oluşan fizyolojik durumu tanımlamada kullanılır. Klinik çalışmalar sonucu elde edilen veriler, sistemik oksidatif stresin metabolik sendrom ve komponentleriyle yakından ilişkili olduğunu göstermektedir. Kronik hiperglisemi ve hiperlipidemi, ROS oluşumu için önemli risk faktörleridir. Hipergliseminin, ROS birikimine katkısı farklı metabolik yolaklar üzerinden gerçekleşebilmektedir. Temel olarak hiperglisemik koşullarda glikolitik yolağın aktivitesinin artması ve mitokondriyal elektron taşıma sistemi üzerinde oluşan elektron basıncı, ROS oluşumuna katkı sağlar. Reaktif oksijen türevlerinin oluşumu ve birikimi daha sonra glikolizde görevli kilit enzimlerden gliseraldehit 3-P dehidrogenaz (GAPDH) enzim aktivitesini baskılayarak hücreyi, glikozu alternatif yolaklarla metabolize etmeye zorlar. Glikoliz ve krebs döngüsünün etkinliği azalır; polyol yolağı, hekzozamin yolağı ve protein kinaz C (PCK) aktivitesi artar. Tüm bu alternatif metabolik yolaklar hücrede ROS oluşumunu daha da artırır. ROS birikimi, insülinin gen ekspresyonunu ve beta hücrelerden insülin salınımını posttranslasyonel faktörler aracılığıyla azaltarak, insülin direnci patogenezine katkı sağlayabilir. Hiperglisemi kaynaklı ROS birikimi, diyabet komplikasyonlarının oluşumunda da önemli role sahiptir. Klinik çalışmaların sonuçları, diyabet ve komplikasyonlarının, hücrenin protein, lipit ve nükleik asit komponentlerinde yarattığı oksidatif hasarı belirlemede pek çok belirtecin kullanılabileceğini ve bu belirteçlerin oksidan harabiyetin düzeyi hakkında fikir verebileceğini göstermektedir.

Kaynakça

  • 1. Robertson RP. Chronic oxidative stress as a central mechanism for glucose toxicity in pancreatic islet beta cells in diabetes. J Biol Chem. 2004;279(41):42351–4.
  • 2. Wright E, Scism-Bacon JL, Glass LC, Glass L. Oxidative stress in type 2 diabetes: the role of fasting and postprandial glycaemia. Int J Clin Pract. 2006;60(3):308–14.
  • 3. Yan L-J. Pathogenesis of chronic hyperglycemia: from reductive stress to oxidative stress. J Diabetes Res. 2014;2014:137919.
  • 4. Lorenzi M. The polyol pathway as a mechanism for diabetic retinopathy: attractive, elusive, and resilient. Exp Diabetes Res. 2007;2007:61038.
  • 5. Tang WH, Martin KA, Hwa J. Aldose Reductase, Oxidative Stress, and Diabetic Mellitus. Front Pharmacol. 2012;3:87.
  • 6. Lee AY, Chung SS. Contributions of polyol pathway to oxidative stress in diabetic cataract. FASEB J. 1999;13(1):23–30.
  • 7. Drel VR, Pacher P, Ali TK, Shin J, Julius U, El-Remessy AB, et al. Aldose reductase inhibitor fidarestat counteracts diabetes-associated cataract formation, retinal oxidative-nitrosative stress, glial activation, and apoptosis. Int J Mol Med. 2008;21(6):667–76.
  • 8. Giacco F, Brownlee M. Oxidative stress and diabetic complications. Circ Res. 2010;107(9):1058–70.
  • 9. Ramirez MA, Borja NL. Epalrestat: An Aldose Reductase Inhibitor for the Treatment of Diabetic Neuropathy. Pharmacotherapy. 2008;28(5):646–55.
  • 10. Giannoukakis N. Drug evaluation: ranirestat--an aldose reductase inhibitor for the potential treatment of diabetic complications. Curr Opin Investig Drugs. 2006;7(10):916–23.
  • 11. Johnson BF, Nesto RW, Pfeifer MA, Slater WR, Vinik AI, Chyun DA, et al. Cardiac abnormalities in diabetic patients with neuropathy: effects of aldose reductase inhibitor administration. Diabetes Care. 2004;27(2):448–54.
  • 12. Schleicher ED, Weigert C. Role of the hexosamine biosynthetic pathway in diabetic nephropathy. Kidney Int. 2000;58(77):13–8.
  • 13. Pantaleon M, Tan HY, Kafer GR, Kaye PL. Toxic effects of hyperglycemia are mediated by the hexosamine signaling pathway and o-linked glycosylation in early mouse embryos. Biol Reprod. 2010;82(4):751–8.
  • 14. Semba RD, Huang H, Lutty GA, Van Eyk JE, Hart GW. The role of O-GlcNAc signaling in the pathogenesis of diabetic retinopathy. Proteomics Clin Appl. 2014;8(3–4):218–31.
  • 15. Horal M, Zhang Z, Stanton R, Virkamäki A, Loeken MR. Activation of the hexosamine pathway causes oxidative stress and abnormal embryo gene expression: Involvement in diabetic teratogenesis. Birth Defects Res Part A - Clin Mol Teratol. 2004;70(8):519–27.
  • 16. Yang X, Ongusaha PP, Miles PD, Havstad JC, Zhang F, So WV, et al. Phosphoinositide signalling links O-GlcNAc transferase to insulin resistance. Nature. 2008;451(7181):964–9.
  • 17. Cooksey RC, Hebert LF, Zhu J-H, Wofford P, Garvey WT, McClain DA. Mechanism of Hexosamine-Induced Insulin Resistance in Transgenic Mice Overexpressing Glutamine:Fructose-6-Phosphate Amidotransferase: Decreased Glucose Transporter GLUT4 Translocation and Reversal by Treatment with Thiazolidinedione 1. Endocrinology. 1999;140(3):1151–7.
  • 18. Soetikno V, Watanabe K, Lakshamanan AP, Arumugam S, Sari FR, Sukumaran V, et al. Role of Protein Kinase C-MAPK, Oxidative Stress and Inflammation Pathways in Diabetic Nephropathy. J Nephrol Ther. 2012;s2(1).
  • 19. Geraldes P, King GL. Activation of Protein Kinase C Isoforms and Its Impact on Diabetic Complications. Circ Res. 2010;106:1319–31.
  • 20. Luo X, Wu J, Jing S, Yan L-J. Hyperglycemic Stress and Carbon Stress in Diabetic Glucotoxicity. Aging Dis. 2016;7(1):90–110.
  • 21. Khaled A. Ahmed Ikram S. SM. Type 2 Diabetes and Vascular Complications: A pathophysiologic view. Biomed Res. 2010;21(2):147–15.
  • 22. Lind M, Odén A, Fahlén M, Eliasson B. The true value of HbA1c as a predictor of diabetic complications: simulations of HbA1c variables. PLoS One. 2009;4(2):e4412.
  • 23. Nagai R, Murray DB, Metz TO, Baynes JW. Chelation: a fundamental mechanism of action of AGE inhibitors, AGE breakers, and other inhibitors of diabetes complications. Diabetes. 2012;61(3):549–59.
  • 24. Kaneto H, Matsuoka T, Katakami N, Kawamori D, Miyatsuka T, Yoshiuchi K, et al. Oxidative stress and the JNK pathway are involved in the development of type 1 and type 2 diabetes. Curr Mol Med. 2007;7(7):674–86.
  • 25. Tabak O, Gelisgen R, Erman H, Erdenen F, Muderrisoglu C, Aral H, et al. Oxidative lipid, protein, and DNA damage as oxidative stress markers in vascular complications of diabetes mellitus. Clin Invest Med. 2011;34(3):E163–71.
  • 26. Dhanasekaran DN, Reddy EP. JNK signaling in apoptosis. Oncogene. 2008;27(48):6245–51.
  • 27. Grankvist K, Marklund SL, Taljedal I-B. CuZn-superoxide dismutase, Mn-superoxide dismutase, catalase and glutathione peroxidase in pancreatic islets and other tissues in the mouse. Biochem J. 1981;199:393–8.
  • 28. Eriksson JW. Metabolic stress in insulin’s target cells leads to ROS accumulation - A hypothetical common pathway causing insulin resistance. FEBS Lett. 2007;581(19):3734–42.
  • 29. Draznin B. Molecular mechanisms of insulin resistance: Serine phosphorylation of insulin receptor substrate-1 and increased expression of p85 α: The two sides of a coin. Diabetes. 2006;55(8):2392–7.
  • 30. Rains JL, Jain SK. Oxidative stress, insulin signaling, and diabetes. Free Radic Biol Med. 2011;50(5):567–75.
  • 31. Bouzakri K, Karlsson HKR, Vestergaard H, Madsbad S, Christiansen E, Zierath JR. IRS-1 serine phosphorylation and insulin resistance in skeletal muscle from pancreas transplant recipients. Diabetes. 2006;55(3):785–91.
  • 32. Bloch-Damti A, Bashan N. Proposed Mechanisms for the Induction of Insulin Resistance by Oxidative Stress. Antioxid Redox Signal. 2005;7(11–12):1553–67.
  • 33. Yang H, Jin X, Kei Lam CW, Yan SK. Oxidative stress and diabetes mellitus. Clin Chem Lab Med. 2011;49(11):1773–82.
  • 34. Safi SZ, Qvist R, Kumar S, Batumalaie K, Ismail IS Bin. Molecular mechanisms of diabetic retinopathy, general preventive strategies, and novel therapeutic targets. Biomed Res Int. 2014;2014:801269.
  • 35. Preedy VR. Aging: Oxidative Stress and Dietary Antioxidants. Aging: Oxidative Stress and Dietary Antioxidants. 2014. 3-13 p.
  • 36. Valavanidis A, Vlachogianni T, Fiotakis C. 8-Hydroxy-2′ -deoxyguanosine (8-OHdG): A critical biomarker of oxidative stress and carcinogenesis. J Environ Sci Heal - Part C Environ Carcinog Ecotoxicol Rev. 2009;27(2):120–39.
  • 37. Martín-Gallán P, Carrascosa A, Gussinyé M, Domínguez C. Biomarkers of diabetes-associated oxidative stress and antioxidant status in young diabetic patients with or without subclinical complications. Free Radic Biol Med. 2003;34(12):1563–74.
  • 38. Bloomer RJ, Fisher-Wellman KH. Blood oxidative stress biomarkers: influence of sex, exercise training status, and dietary intake. Gend Med. 2008;5(3):218–28. 39. Il’yasova D, Scarbrough P, Spasojevic I. Urinary biomarkers of oxidative status. Clin Chim Acta. 2012;413(19–20):1446–53.
  • 40. Frijhoff J, Winyard PG, Zarkovic N, Davies SS, Stocker R, Cheng D, et al. Clinical Relevance of Biomarkers of Oxidative Stress. Antioxid Redox Signal. 2015;23(14):1144–70.
  • 41. Zujko ME., Witkowska AM., Górska M., Wilk J., Kretowski A. Reduced intake of dietary antioxidants can impair antioxidant status in type 2 diabetes patients. Pol Arch Med Wewn. 2014;124(11):599–607.
  • 42. Zhang Y, Du Y, He J-F, Li K-J. 8-iso-prostaglandin-F2α: a possible trigger or accelerator of diabetic retinopathy. Int J Ophthalmol. 2016;9(1):163–5.
  • 43. Pandey KB, Mishra N, Rizvi SI. Protein oxidation biomarkers in plasma of type 2 diabetic patients. Clin Biochem. 2010;43(4–5):508–11.
  • 44. Chao M-R, Rossner P, Haghdoost S, Jeng HA, Hu C-W, Hu C-W. Nucleic acid oxidation in human health and disease. Oxid Med Cell Longev. 2013;2013:368651.
  • 45. Liu X, Gan W, Zou Y, Yang B, Su Z, Deng J, et al. Elevated Levels of Urinary Markers of Oxidative DNA and RNA Damage in Type 2 Diabetes with Complications. 2016;2016.
  • 46. Pan H, Zhang L, Guo M, Sui H, Li H, Wu W, et al. The oxidative stress status in diabetes mellitus and diabetic nephropathy. Acta Diabetol. 2010;47(S1):71–6.
Toplam 45 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Konular Sağlık Kurumları Yönetimi
Bölüm Derleme
Yazarlar

Özlem Çetiner 0000-0001-9872-416X

Neslişah Rakıcıoğlu Bu kişi benim 0000-0001-8763-7407

Yayımlanma Tarihi 23 Nisan 2020
Kabul Tarihi 22 Nisan 2020
Yayımlandığı Sayı Yıl 2020 Cilt: 4 Sayı: 1

Kaynak Göster

APA Çetiner, Ö., & Rakıcıoğlu, N. (2020). Hiperglisemi, Oksidatif Stres ve Tip 2 Diyabette Oksidatif Stres Belirteçlerinin Tanımlanması. Türkiye Diyabet Ve Obezite Dergisi, 4(1), 60-68. https://doi.org/10.25048/tudod.638744
AMA Çetiner Ö, Rakıcıoğlu N. Hiperglisemi, Oksidatif Stres ve Tip 2 Diyabette Oksidatif Stres Belirteçlerinin Tanımlanması. Turk J Diab Obes. Nisan 2020;4(1):60-68. doi:10.25048/tudod.638744
Chicago Çetiner, Özlem, ve Neslişah Rakıcıoğlu. “Hiperglisemi, Oksidatif Stres Ve Tip 2 Diyabette Oksidatif Stres Belirteçlerinin Tanımlanması”. Türkiye Diyabet Ve Obezite Dergisi 4, sy. 1 (Nisan 2020): 60-68. https://doi.org/10.25048/tudod.638744.
EndNote Çetiner Ö, Rakıcıoğlu N (01 Nisan 2020) Hiperglisemi, Oksidatif Stres ve Tip 2 Diyabette Oksidatif Stres Belirteçlerinin Tanımlanması. Türkiye Diyabet ve Obezite Dergisi 4 1 60–68.
IEEE Ö. Çetiner ve N. Rakıcıoğlu, “Hiperglisemi, Oksidatif Stres ve Tip 2 Diyabette Oksidatif Stres Belirteçlerinin Tanımlanması”, Turk J Diab Obes, c. 4, sy. 1, ss. 60–68, 2020, doi: 10.25048/tudod.638744.
ISNAD Çetiner, Özlem - Rakıcıoğlu, Neslişah. “Hiperglisemi, Oksidatif Stres Ve Tip 2 Diyabette Oksidatif Stres Belirteçlerinin Tanımlanması”. Türkiye Diyabet ve Obezite Dergisi 4/1 (Nisan 2020), 60-68. https://doi.org/10.25048/tudod.638744.
JAMA Çetiner Ö, Rakıcıoğlu N. Hiperglisemi, Oksidatif Stres ve Tip 2 Diyabette Oksidatif Stres Belirteçlerinin Tanımlanması. Turk J Diab Obes. 2020;4:60–68.
MLA Çetiner, Özlem ve Neslişah Rakıcıoğlu. “Hiperglisemi, Oksidatif Stres Ve Tip 2 Diyabette Oksidatif Stres Belirteçlerinin Tanımlanması”. Türkiye Diyabet Ve Obezite Dergisi, c. 4, sy. 1, 2020, ss. 60-68, doi:10.25048/tudod.638744.
Vancouver Çetiner Ö, Rakıcıoğlu N. Hiperglisemi, Oksidatif Stres ve Tip 2 Diyabette Oksidatif Stres Belirteçlerinin Tanımlanması. Turk J Diab Obes. 2020;4(1):60-8.

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