Complication of Diabetes

Yıl 2024, Cilt: 19 Sayı: 3, 162 - 166, 04.11.2024

Nazlıcan İğci , Nurten Seringeç Akkeçeci

https://doi.org/10.17517/ksutfd.1239400

Öz

Diabetes (DM) is a heterogeneous metabolic disorder characterized by chronic hyperglycemia caused by impaired insulin secretion impaired insulin action, or usually both. Diabetes-related complications resulting from hyperglycemia are quite common and are responsible for many morbidity and mortality. The main cause of tissue damage due to diabetes is hyperglycemia. When most cells are exposed to hyperglycemia, it can keep the intracellular glucose concentration constant by reducing intracellular glucose transport. Capillary endothelial cells in the retina, mesangial cells in the renal glomerulus, neurons in peripheral nerves, and Schwann cells are the most damaged cells in hyperglycemia. Because when these cells are exposed to hyperglycemia, they cannot decrease the intracellular glucose transport, and the intracellular glucose concentration increases in these cells. As a result of high glucose concentration, changes occur in cellular mechanisms. Cellular mechanisms causing complications of diabetes; increased polyol pathway flux, intracellular production of advanced glycation end products (AGE), protein kinase C (PKC) activation, and increased hexosamine pathway activity. Complications of diabetes are divided into acute and chronic complications. Acute complications of diabetes are hyperglycemia, diabetic ketoacidosis, hyperosmolar coma, and hypoglycemia. Chronic complications of diabetes are divided into microvascular and macrovascular complications. Microvascular complications include neuropathy, nephropathy, and retinopathy. Macrovascular complications are cardiovascular diseases, stroke, and peripheral vascular diseases. The purpose of this review is to provide information about the complications of diabetes and the cellular mechanisms that cause diabetes complications.

Anahtar Kelimeler

Diabetes, Acute complications, Chronic complications, Cellular mechanisms

Diyabetin Komplikasyonları

Öz

Diyabet (DM), bozulmuş insülin sekresyonu veya bozulmuş insülin etkisi ya da genellikle her ikisinin meydana geldiği kronik hiperglisemi ile karakterize heterojen metabolik bir bozukluktur. Hiperglisemi sonucu meydana gelen diyabete bağlı komplikasyonlar oldukça yaygındır ve birçok morbidite ve mortaliteden sorumludur. Diyabete bağlı oluşan doku hasarının ana nedeni hiperglisemidir. Çoğu hücre hiperglisemiye maruz kaldığında hücre içi glikoz taşınmasını azaltarak hücre içi glikoz konsantrasyonunu sabit tutabilmektedir. Retinadaki kılcal endotelyal hücreler, renal glomerulustaki mezengiyal hücreler, periferik sinirlerdeki nöronlar ve Schwann hücreleri hiperglisemide en çok zarar gören hücrelerdir. Çünkü bu hücreler hiperglisemiye maruz kaldıklarında hücre içi glikoz taşınmasını azaltamazlar ve bu hücrelerde hücre içi glikoz konsantrasyonu artar. Glikoz konsantrasyonunun yüksek olması sonucunda da hücresel mekanizmalarda değişiklikler gerçekleşir. Diyabetin komplikasyonlarına sebep olan hücresel mekanizmalar; artan polyol yolu akışı, ilerlemiş glikasyon son ürünlerinin (AGE) hücre içi üretimi, protein kinaz C (PKC) aktivasyonu ve artan heksozamin yolu aktivitesidir. Diyabetin komplikasyonları akut ve kronik komplikasyonlar olmak üzere ikiye ayrılır. Diyabetin akut komplikasyonları hiperglisemi, diyabetik ketoasidoz, hiperozmolar koma ve hipoglisemidir. Diyabetin kronik komplikasyonları mikrovasküler ve makrovasküler komplikasyonlar olarak kendi içinde ayrılmaktadır. Mikrovasküler komplikasyonlar arasında nöropati, nefropati ve retinopati bulunmaktadır. Makrovasküler komplikasyonlar ise kardiyovasküler hastalıklar, felç ve periferik vasküler hastalıklardır. Bu derlemenin amacı, diyabetin komplikasyonları ve diyabetin komplikasyonlarına sebep olan hücresel mekanizmalar hakkında bilgi vermektir.

Anahtar Kelimeler

Diyabet, Akut komplikasyonlar, Kronik komplikasyonlar, Hücresel mekanizmalar

Kaynakça

• Petersmann A, Müller-Wieland D, Müller UA, Landgraf R, Nauck M, Freckmann G, et al. Definition, Classification and Diagnosis of Diabetes Mellitus. Experimental and Clinical Endocrinology & Diabetes. 2019;127(01):1–7.
• Classification and diagnosis of diabetes: Standards of medical care in diabetes-2021. Diabetes Care. 2021 Jan;44(1):15–33.
• Papatheodorou K, Banach M, Bekiari E, Rizzo M, Edmonds M. Complications of Diabetes 2017. J Diabetes Res. 2018;2018:1–4.
• Zheng Y, Ley SH, Hu FB. Global aetiology and epidemiology of type 2 diabetes mellitus and its complications. Nat Rev Endocrinol. 2018;14(2):88–98.
• Brownlee M. The pathobiology of diabetic complications: a unifying mechanism. Diabetes. 2005;54(6):1615–1625.
• Lee AY, Chung SS. Contributions of polyol pathway to oxidative stress in diabetic cataract. FASEB J. 1999;13(1):23–30.
• Ishii H, Jirousek MR, Koya D, Takagi C, Xia P, Clermont A, et al. Amelioration of vascular dysfunctions in diabetic rats by an oral PKC beta inhibitor. Science. 1996;272(5262):728–731.
• Kolm-Litty V, Sauer U, Nerlich A, Lehmann R, Schleicher ED. High glucose-induced transforming growth factor beta1 production is mediated by the hexosamine pathway in porcine glomerular mesangial cells. Journal of Clinical Investigation. 1998;101(1):160–169.
• Clark RJ, McDonough PM, Swanson E, Trost SU, Suzuki M, Fukuda M, et al. Diabetes and the accompanying hyperglycemia impairs cardiomyocyte calcium cycling through increased nuclear O-GlcNAcylation. Journal of Biological Chemistry. 2003;278(45):44230–44237.
• McPhee SJ, Lingappa VR, Ganong WF. Endokrin Pankreas Bozuklukları. Erkan Çoban, Gültekin Süleymanlar. Hastalıkların Patofizyolojisi, 4.Baskı, Ankara, Palme Yayıncılık, 2006;516-526.
• Modi A, Agrawal A, Morgan F. Euglycemic diabetic ketoacidosis: a review. Curr Diabetes Rev. 2017;13(3):315–321.
• Fayfman M, Pasquel FJ, Umpierrez GE. Management of hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Medical Clinics of North America. 2017;101(3):587–606.
• Hassan EM, Mushtaq H, Mahmoud EE, Chhibber S, Saleem S, Issa A, et al. Overlap of diabetic ketoacidosis and hyperosmolar hyperglycemic state. World J Clin Cases. 2022;10(32):11702–11711.
• Benjamin IJ, Giriggs RC, Wing EJ, Fitz G. Diabetes Mellitus, Hipoglisemi. Serhat Ünal. Cecil Essentials of Medicine. 9.Baskı, Ankara, Güneş Tıp Kitabevleri, 2016;68-670.
• Pasquel FJ, Umpierrez GE. Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment. Diabetes Care. 2014;37(11):3124–3131.
• Ağar E. Endokrin Pankreas. İnsan Fizyolojisi. 1.Baskı, İstanbul, İstanbul Tıp Kitabevleri, 2021;968.
• Skyler JS, Bakris GL, Bonifacio E, Darsow T, Eckel RH, Groop L, et al. Differentiation of diabetes by pathophysiology, natural history, and prognosis. Diabetes. 2017;66(2):241–255.
• Deshpande AD, Harris-Hayes M, Schootman M. Epidemiology of diabetes and diabetes-related complications. Phys Ther. 2008;88(11):1254–1264.
• Hardigan T, Ward R, Ergul A. Cerebrovascular complications of diabetes: focus on cognitive dysfunction. Clin Sci. 2016;130(20):1807–1822.
• Forbes JM, Cooper ME. Mechanisms of diabetic complications. Physiol Rev. 2013;93(1):137–188.
• Gorelick PB, Scuteri A, Black SE, DeCarli C, Greenberg SM, Iadecola C, et al. Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the american heart association/american stroke association. Stroke. 2011;42(9):2672–2713.
• Papatheodorou K, Banach M, Edmonds M, Papanas N, Papazoglou D. Complications of diabetes. J Diabetes Res. 2015;2015:1–5.
• Hellmich B, Schellner M, Schatz H, Pfeiffer A. Activation of transforming growth Factor-131 in diabetic kidney disease. Metabolism. 2000;49(3):353–359.
• Samsu N. Diabetic nephropathy: challenges in pathogenesis, diagnosis, and treatment. Biomed Res Int. 2021;2021:1–17.
• Santos KG, Crispim D, Canani LH, Ferrugem PT, Gross JL, Roisenberg I. Relationship of endothelial nitric oxide synthase (eNOS) gene polymorphisms with diabetic retinopathy in Caucasians with type 2 diabetes. Ophthalmic Genet. 2012;33(1):23–27.
• Frank RN. Diabetic retinopathy. New England Journal of Medicine. 2004;350(1):48–58.
• Hall JE. İnsülin, Glukagon ve Diyabetes Mellitus. Berrak Çağlayan Yeğen. Guyton ve Hall Tıbbi Fizyoloji. 13.Baskı, Ankara, Güneş Tıp Kitabevleri, 2017;996.
• Huang D, Refaat M, Mohammedi K, Jayyousi A, Al Suwaidi J, Abi Khalil C. Macrovascular complications in patients with diabetes and prediabetes. Biomed Res Int. 2017;2017:1–9.
• Volmer-Thole M, Lobmann R. Neuropathy and diabetic foot syndrome. Int J Mol Sci. 2016;17(6):917.