精胺氧化酶介导的多胺分解代谢在高血糖和糖尿病发病及治疗中的作用

Alford Ahmed Sean
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摘要

糖尿病是一种慢性的、与葡萄糖和胰岛素有关的病理生理调节的内分泌功能紊乱的疾病。高血糖是这种功能障碍最常见和密切相关的并发症,有无数的致病性方法。高血糖有能力加剧关键组织中的退行性正反馈循环。考虑到胰腺激素调节在血清葡萄糖稳态中起着越来越重要的作用,在这里,我们开始讨论多胺分解代谢作为一种途径的含义,其机制将在很大程度上促进胰腺胰岛细胞的坏死和功能障碍。这种机制的致病性主要集中在高血糖诱导自由基产生的持续增加如何减轻糖尿病的几种并发症。精胺氧化为亚精胺产生过氧化氢,以及3-氨基丙醇(自发转化为丙烯醛)和亚精胺(该反应底物的前体)。这种活性氧的增加显示出抑制自噬和细胞凋亡以及刺激胰腺细胞内脂肪坏死的能力。考虑到胰腺的胰岛细胞在葡萄糖稳态中起着极其重要的作用,这些ROS浓度的微小变化能够消除大的调节因子,而在疾病过程和治疗分析中却未被发现。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Polyamine catabolism via spermine oxidase in the pathogenesis and treatment of hyperglycemia and diabetes mellitus-A short discussion
Diabetes mellitus can be described as chronic, endocrine dysfunction of pathophysiological regulation related to glucose and insulin. Hyperglycemia is the most common and intensely related complication of this dysfunction and has countless methods of pathogenicity. Hyperglycemia has the ability to exacerbate a degenerative positive feedback loop within critical tissues. Considering the fact that pancreatic hormonal regulation has played an increasingly considerable role in serum glucose homeostasis, here we begin a discussion into the implication of polyamine catabolism as a pathway with a mechanism that would contribute considerably to the necrosis and dysfunction of islet cells in the pancreas. The pathogenicity of this mechanism focuses on how the sustained increase in free radical production by hyperglycemic induction extenuates several complications in diabetes mellitus. The oxidation of spermine to spermidine produces hydrogen peroxide, as well as 3-aminopropanol (which spontaneously converts to acrolein) and spermidine (the precursor for the substrate of this reaction). This increase in reactive oxygen species exhibits the ability to inhibit autophagy and apoptosis as well as stimulate fat necrosis within the cells of the pancreas. Considering the islet cells of the pancreas play an extremely important role in glucose homeostasis, small changes in concentrations of these ROS are able to eliminate large regulatory factors while going undetected in the analysis of disease processes and therapeutics.
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