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[蛋白质的非酶糖基化。糖尿病、衰老和肾衰竭的并发症]

[Non-enzymatic glycosylation of proteins. Complications of diabetes mellitus, aging and kidney failure].

作者信息

Monnier V

机构信息

Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106.

出版信息

Presse Med. 1993 Oct 9;22(30):1413-8.

PMID:8248084
Abstract

Non-enzymatic protein glycosylation is the first stage of the reaction described by L.C. Maillard. When the reaction progresses beyond that stage the long half-life molecules are damaged by formation of intermolecular crosslinking. The recent discovery of pentosidine, a crosslink between lysine and arginine residues, has demonstrated that advanced Maillard reaction is accelerated in diabetic patients with severe complications. Moreover, high tissue and plasma levels of pentosidine have been found in uraemia. The formation of advanced Maillard end-products (AGE) in plasma proteins constitutes a source of cell stimulation which induces macrophages to secrete cytokines, interleukin-1 and tumoral necrosis factor. Similarly, endothelial cells are induced to increase the permeability and production of the procoagulant factor. These mechanisms are thought to play an important role in the pathogenesis of atherosclerosis, nephropathy and thromboembolic disorders of diabetes. The discovery of beneficial effects of amino-guanidine, an inhibitor of advanced Maillard reaction, in the prevention of experimental diabetic complications opens a new line of investigation and new hopes for diabetics.

摘要

非酶蛋白糖基化是L.C. 美拉德所描述反应的第一阶段。当反应超过该阶段时,长半衰期分子会因分子间交联的形成而受损。近期对戊糖苷(赖氨酸和精氨酸残基之间的一种交联物)的发现表明,严重并发症的糖尿病患者体内晚期美拉德反应会加速。此外,在尿毒症患者中已发现组织和血浆中戊糖苷水平较高。血浆蛋白中晚期美拉德终产物(AGE)的形成构成了细胞刺激源,可诱导巨噬细胞分泌细胞因子、白细胞介素 -1和肿瘤坏死因子。同样,内皮细胞被诱导增加通透性和促凝血因子的产生。这些机制被认为在糖尿病的动脉粥样硬化、肾病和血栓栓塞性疾病的发病机制中起重要作用。晚期美拉德反应抑制剂氨基胍在预防实验性糖尿病并发症方面有益作用的发现,为糖尿病研究开辟了新的途径并带来了新的希望。

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