scholarly journals The role of glycation end products in the development and progression of diabetic neuroarthropathy

2021 ◽  
Vol 67 (3) ◽  
pp. 4-9
Author(s):  
M. M. Kalandiya ◽  
A. Yu. Tokmakova ◽  
G. R. Galstyan

Diabetic neuroarthropathy (DNOAP, Charcot’s foot) is a serious complication of diabetes mellitus, the genesis of which is not fully understood. In most cases, this pathology is diagnosed late, which leads to the development of severe deformities of the foot, up to the loss of support ability of the limb. There is no single hypothesis for the formation of Charcot’s foot, but there are factors predisposing to its development, as well as a few likely provoking events. Excessive formation and accumulation of end products of glycation may play an important role in the pathogenesis of this complication of diabetes. End products of glycation (AGE) are a variety of compounds formed as a result of a non-enzymatic reaction between carbohydrates and free amino groups of proteins, lipids and nucleic acids. There are various factors that lead to the accumulation of AGE in the human body. Allocate endogenous and exogenous factors. The former include certain diseases, such as diabetes mellitus, renal failure, which accelerate glycation processes. Exogenous factors leading to the formation of lipo-oxidation and glyco-oxidation products include tobacco smoke and prolonged heat treatment of food.This review provides information on the role of glycation end products in the development and progression of complications in patients with diabetes mellitus.

2003 ◽  
Vol 31 (6) ◽  
pp. 1400-1402 ◽  
Author(s):  
M. Bourajjaj ◽  
C.D.A. Stehouwer ◽  
V.W.M. van Hinsbergh ◽  
C.G. Schalkwijk

Various theories have been proposed to explain the hyperglycaemia-induced pathogenesis of vascular complications of diabetes, including detrimental effects of AGEs (advanced glycation end products) on vascular tissues. Increased formation of the very reactive dicarbonyl compound MGO (methylglyoxal), one of the side-products of glycolysis, and MGO-derived AGEs seem to be implicated in the development of diabetic vascular complications. Although the exact role of MGO and MGO adducts in the development of vascular complications is unknown, receptor-mediated activation of vascular cells by the MGO–arginine adduct hydroimidazolone, as well as intracellular modifications of protein by MGO, seem to be involved. The aim of this mini-review is to assess to what extent MGO is related to vascular complications in diabetes.


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