Journals / Bezmiâlem Science / 2019 / Cilt: 7 - Sayı: 1

Diabetes, Oxidative Stress and Endothelial Dysfunction

Diyabet, Oksidatif Stres ve Endotel Disfonksiyonu

Pages
52–57
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Thus, endothelial dysfunction may be ameliorated and diabetic vascular complications can be avoided.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Cardiovascular diseases are the most common causes of morbidity and mortality in diabetic patients.
📊
Key Findings & Data:Under conditions of oxidative stress, free oxygen radicals may increase insulin resistance and affect pancreatic beta cells.
💡
Conclusion & Impact:Thus, endothelial dysfunction may be ameliorated and diabetic vascular complications can be avoided.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Cardiovascular diseases are the most common causes of morbidity and mortality in diabetic patients. Oxidative stress plays an important role in diabetic endothelial dysfunction. Under conditions of oxidative stress, free oxygen radicals may increase insulin resistance and affect pancreatic beta cells. Several experimental animal models to understand the pathogenesis of diabetes mellitus have been developed, and the model including high fat diet which leads to insulin resistance is the best animal model to mimic type 2 diabetes mellitus. In diabetes mellitus, it is well known that there is an increase in lipid peroxidation. This condition is also associated with oxidative stress. Endothelial dysfunction creates imbalance between vasoconstriction and vasodilatation. In large arteries, nitric oxide plays a main role in endothelium-dependent vasodilatation. Abnormal production or response of nitric oxide contributes vascular and endothelial dysfunction in diabetes mellitus. Oxidative stress reduces the levels of nitric oxide and diminishes endothelium- dependent vasodilatation. Therefore, in recent years, the studies to treat the diabetic complications have focused on antioxidant agents. The goal of the treatment is to decrease oxidative stress, as well as lipid and glucose levels. Thus, endothelial dysfunction may be ameliorated and diabetic vascular complications can be avoided.

Özet

Kardiyovasküler hastalıklar, diyabetik hastalarda en sık görülen morbidite ve mortalite nedenidir. Diyabette endotel disfonksiyonunda oksidatif stres önemli bir rol oynamaktadır. Oksidatif stres durumlarında, serbest oksijen radikalleri insülin direncini artırıp pankreas beta hücrelerini de etkileyebilir. Diyabetin patogenezinin anlaşılmasında çeşitli deneysel modeller hayvanlarda oluşturulmakta olup özellikle yağlı diyet içerenler, insülin direnci oluşturduğundan tip 2 diyabeti en iyi taklit eden modellerdir. Diyabette lipid peroksidasyonunda da bir artış olduğu bilinmektedir. Bu durum yine oksidatif stresle ilişkilidir. Diyabette endotel disfonksiyonu, vazokonstrüksiyon ve vazodilatasyon arasında dengesizlikle kendini gösterir. Büyük boy arterlerde nitrik oksit, endotele bağlı gevşemede ana rolü üstlenmektedir. Nitrik oksidin anormal üretimi ya da yanıtı diyabette görülen vasküler ve endotel disfonksiyona katkıda bulunmaktadır. Oksidatif stres, nitrik oksit düzeylerini azaltır ve endotel bağımlı vazodilatasyonun bozulmasına neden olur. Bu nedenle son yıllarda diyabetik komplikasyonların tedavisine yönelik araştırmalar antioksidan maddelere odaklanmıştır. Tedavide amaç oksidatif stresi, lipid ve glikoz düzeylerini düşürmektir. Böylelikle endotel disfonksiyonu iyileştirilip diyabete bağlı vasküler komplikasyonların önüne geçilebilir.

🔖

Cite This Article

ÖZTÜRK, Z. (2019). Diabetes, Oxidative Stress and Endothelial Dysfunction. Bezmiâlem Science, Cilt: 7 - Sayı: 1, 52–57. https://ajindex.com/articles/147283

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (13)

  1. Larner J. Insulin and oral hypoglysemic drugs, glucagon. In: Gilman AG, Goodman LS, Rall TW, Murad F, editors. Goodman and Gilmans the pharmacological basis therapeutics. New York: MacMillan Publ. Comp; 1985.p.1490-516.
  2. Özata M, Yöntem A. Endokrinoloji metabolizma ve diabet. 1st ed. Istanbul: Istanbul Medikal; 2006.
  3. Satman I, Yilmaz T, Sengül A, Salman S, Salman F, Uygur S, et al. Population-based study of diabetes and risk characteristics in Turkey: results of the turkish diabetes epidemiology study (TURDEP). Diabetes Care. 2002;25:1551-6.
  4. Wilson JD, Foster DW, Kronenberg HM, Larsen PR. Williams Textbook of Endocrinology. 9th ed. Philadelphia: WB. Saunders Company; 1998.
  5. Scarlett JA, Gray RS, Griffin J, Olefsky JM, Kolterman OG. Insulin teatment reverses the insulin resistance of type II diabetes mellitus. Diabetes Care 1982;5:353-63.
  6. Wing RR, Blair EH, Bononi P, Marcus MD, Watanabe R, Bergman RN. Caloric restriction per se is a significant factor in improvements in glycemic control and insulin sensitivity during weight loss in obese NIDDM patients. Diabetes Care 1994;17:30-6. Roden M. Diabetes mellitus: definition, classification and diagnosis. Acta Med Austriaca 2004;31:156-7. Kannel WB. Contribution of the Framingham Study to the Coquest of Coronary Artery Disease. Am J Cardiol 1988;62:1109-12.
  7. Dunn JS, Duffy E, Gilmour MK, Kirkpatrick J, McLetchie NGB. Further observations on the effects of alloxan on the pancreatic islets. J Physiol 1944;103:233-43.
  8. Pushparaj P, Tan CH, Tan BKH. Effects of Averrhoa bilimbi leaf extract on blood glucose and lipids in streptozotocin diabetic rats. J Ethnopharmacol 2000;72:69-76.
  9. Kohnert KD, Axcrona UM, Hehmke B, Klöting I, Sundler F, Ahrén B. Islet neuronal abnormalities associated with impaired insulin secretion in type 2 diabetes in the Chinese hamster. Regul Pept 1999;82:71-9.
  10. Chang AY, Perry CS. Acid glycohydrolase in Chinese hamster with spontaneous diabetes: iv. Diabetes and line dependent variation in plasma enzyme activity. Diabetologia 1978;15:423-9.
  11. Ejrnaes M, Von Errath MG, Christen U. Cure of chronic viral infection and virus-induced type 1 diabetes by neutralizing antibodies. Clin Dev Immunol 2006;13:67-77.
  12. Sahin K, Onderci M, Tuzcu M, Ustundag B, Cikim G, Ozercan IH,et al. Effect of chromium on carbohydrate and lipid metabolism in a rat model of type 2 diabetes mellitus: the fat-fed, streptozotocin- treated rat. Metabolism 2007;56:1233-40.
  13. Zhao S, Chu Y, Zhang C, Lin Y, Xu K, Yang P, et al. Diet-induced c