Complication of Diabetes

Year 2024, Volume: 19 Issue: 3, 162 - 166, 04.11.2024

Nazlıcan İğci , Nurten Seringeç Akkeçeci

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

Abstract

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.

Keywords

Diabetes, Acute complications, Chronic complications, Cellular mechanisms

Diyabetin Komplikasyonları

Abstract

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.

Keywords

Diyabet, Akut komplikasyonlar, Kronik komplikasyonlar, Hücresel mekanizmalar

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