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Low Plasma Albumin Levels are Associated with Increased Plasma Protein Glycation and HbAlc in Diabetes

机译:低血浆白蛋白水平与糖尿病患者血浆蛋白糖基化和HbAlc升高有关

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摘要

Diabetes is characterized by increased levels of plasma glucose, which in turn modifies the blood plasma proteins by a non-enzymatic reaction called glycation. Protein glycation leads to formation of toxic fluorescent molecules called Advanced Glycation End products (AGEs). Formation of AGEs causes cell damage at various levels: a) The protein structure and function is altered b) AGE modified plasma proteins interact with the Receptor for AGEs (RAGE) and activate pro-inflammatory pathway c) AGE modification is associated with protein aggregation fibril formation and protease resistance d) AGE modification leads to dysfunction of extracellular matrix. Accumulation of AGEs has been found to be accelerated in diabetes and to contribute substantially to the progression of diabetic complications including nephropathy, retinopathy, neuropathy, cardiovascular diseases, accelerated aging, cataract, neurodegenerative diseases such as Alzheimer's, Parkinson's disease and amyotrophic lateral sclerosis.
机译:糖尿病的特征是血浆葡萄糖水平升高,这又通过称为糖化作用的非酶促反应改变了血浆蛋白。蛋白质糖基化会导致形成有毒的荧光分子,称为高级糖基化终产物(AGEs)。 AGEs的形成会在不同水平上引起细胞损伤:a)蛋白质结构和功能发生改变b)AGE修饰的血浆蛋白与AGEs受体(RAGE)相互作用并激活促炎途径c)AGE修饰与蛋白聚集原纤维相关d)AGE修饰导致细胞外基质功能异常。已经发现,AGEs的积累在糖尿病中被加速,并且对包括糖尿病,肾病,视网膜病,神经病,心血管疾病,加速衰老,白内障,神经退行性疾病如阿尔茨海默氏病,帕金森氏病和肌萎缩性侧索硬化症的糖尿病并发症的发展有重大贡献。

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