醛糖还原酶抑制剂对stz -糖尿病大鼠多元醇积累的影响

Q4 Medicine
D. Yue
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引用次数: 0

摘要

糖尿病性神经病变的发病机制尚不完全清楚。山梨糖醇的积累被认为是神经病变的一个重要原因。然而,糖尿病周围神经肌醇缺乏也被认为是神经病变的原因之一。山梨糖醇积累和肌醇缺乏的相对重要性尚不清楚,这两个过程通常被认为是独立的现象。在链脲佐菌素糖尿病大鼠中,山梨醇(5mg/kg体重)可使这两种代谢物的浓度正常化。这些结果表明,这两个过程是相互关联的。神经肌醇的缺乏也可以在半乳糖血症大鼠中表现出来,这也可以通过醛糖还原酶抑制而正常化。这些结果表明山梨糖醇或半乳糖醇的积累是导致肌醇缺乏的主要原因。山梨糖醇与肌醇代谢关系的发现,为糖尿病神经病变发病机制中糖尿病神经的两种异常提供了统一的概念。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Polyols Accumulation and Effect of Aldose Reductase Inhibitor in STZ-Diabetic Rats
The pathogenesis of diabetic neuropathy is incompletely understood. The accumulation of sorbitol has been postulated to be an important cause of the neuropthy. However, deficiency of myoinositol in diabetic peripheral nerves has also been documented and suggested as a cause of the neuropathy. The relative importance of sorbitol accumulation and myoinositol deficiency is not known and these two processes have usually been regarded as independent phenomena. In Streptozotocin diabetic rats, the centrations con of these two metabolites can be normalized by treatment with Sorbinil (5mg/kg body weight). These results suggest that the two processes are inter-related. The deficiency of nerve myoinositol can also be demonstrated in galactosaemic rats and again this can be normalized by aldose reductase inhibition. These results suggest that sorbitol or galactitol accumulations are primary events which lead to myoinositol deficiency. The finding of a relationship between sorbitol and myoinositol metabolism provide a unified concept relating the two abnormalities of diabetic nerve in the pathogenesis of diabetic neuropathy.
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来源期刊
Journal of the Japan Diabetes Society
Journal of the Japan Diabetes Society Medicine-Internal Medicine
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