2型糖尿病伴神经病变患者的脂质过氧化物。

I N Migdalis, P Triantafilou, E Petridou, N Varvarigos, V Totolos, A Rigopoulos
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引用次数: 0

摘要

糖尿病及其周围神经代谢变化导致一氧化氮生成减少和神经血流量减少。由于脂质过氧化物被认为是由自由基形成的,并可能在血管疾病的发展中发挥重要作用,我们研究了脂质过氧化物(以硫代巴比妥酸反应物质(TBARS)测量)在糖尿病周围神经病变患者中的可能关系。研究对象为77例2型糖尿病患者(39例为神经性糖尿病,38例为非神经性糖尿病)和38例对照组。神经病变研究组TBARS水平显著低于对照组,为3.5micromol/l(2.2-5.6, 95%置信限),对照组为4.5 micromol/l (3.08-6.8), p < 0.001;无神经病变糖尿病患者TBARS水平为4.9micromol/l (3.09-8.05), p < 0.001。两组糖尿病患者在代谢控制方面没有发现差异。神经病变组神经功能障碍评分与TBARS水平呈负相关(r = - 0.42, p < 0.01)。总之,伴有神经病变的糖尿病患者存在TBARS水平异常。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Lipid peroxides in type 2 diabetic patients with neuropathy.

Diabetes and its metabolic changes in peripheral nerves contribute to cause a decrease of nitric oxide production and diminished nerve blood flow. Since lipid peroxides are thought to be formed by free radicals and may play an important role in the development of vascular disease, we have investigated the possible relationship between lipid peroxides (measured as thiobarbitouric acid reacting substances (TBARS) in diabetic patients with peripheral neuropathy. Seventy-seven patients with Type 2 diabetes (39 neuropathic and 38 non-neuropathic) and 38 control subjects were studied. The neuropathy study group had significantly lower levels of TBARS, 3.5micromol/l (2.2-5.6, 95% confidence limits) compared to controls 4.5microm/l (3.08-6.8), p < 0.001 and to diabetics without neuropathy 4.9micromol/l (3.09-8.05), p < 0.001. No differences were found in metabolic control between the two diabetic groups. In the neuropathy group there was a negative correlation between the score for nerve dysfunction with the TBARS levels (r = - 0.42, p < 0.01). In conclusion, in diabetic patients with neuropathy there are abnormalities of TBARS levels.

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