氧化应激与 1 型糖尿病早期自主神经功能。
Oxidative stress and autonomic nerve function in early type 1 diabetes.
机构信息
LSU Medical School, Shreveport, LA, USA.
出版信息
Clin Auton Res. 2011 Feb;21(1):19-28. doi: 10.1007/s10286-010-0084-4. Epub 2010 Sep 25.
INTRODUCTION
The biochemical mechanisms by which hyperglycemia causes microvascular disease and neuropathy are poorly understood. Experimental studies have established that oxidative stress is present in diabetic rodents with neuropathy, and that antioxidant therapy is protective. Oxidative stress is also present in human diabetes, but its clinical importance is uncertain.
MATERIAL AND METHODS
We examined several biochemical measures of oxidative stress in 37 patients with recent-onset (less than 2 years) type 1 diabetes annually in a 3-year longitudinal study. We also performed a comprehensive annual evaluation of somatosensory and autonomic nerve function. A total of 41 control subjects were studied.
RESULTS
Malondialdehyde excretion, a measure of lipid peroxidation, was 1.5l ± .1 μmol/g creatinine in the control subjects, but 2.43 ± . 3 in the diabetic patients in year one, 2.39 ± .2 in year two and 1.92 ± .15 in year three, which was different from controls across all years; p < .005. Serum NOx (nitrate and nitric) was 34.0 ± 4.9 μmol/L in the controls, but 52.4 ± 5 in the diabetics in year one, 50.0 ± 5.1 in year two, and 49.0 ± 5.2 in year three, which was different from controls; p < .01. We measured sudomotor function and observed that the poorly controlled diabetic patients had relatively increased sweating above the waist and relatively decreased sweating below the waist, a typical pattern for sympathetic nerve injury. The ratio of sweating above to sweating below the waist was .385 ± .04 in controls, 0.70 ± .14 in diabetic patients in year one, .51 ± .14 in year two and .496 ± .12 in year three (different from controls; p < .01 across all years). Urinary MDA correlated negatively with total sweat (r = -39, p < .01); NOx also correlated negatively with total sweat (r = -.34, p < .025). Abnormalities in the processing of renin (the renin/prorenin ratio), a test of renal sympathetic neurons, was also documented in early type 1 diabetes.
CONCLUSIONS
Oxidative stress and excessive serum NOx are associated with sympathetic dysfunction in early type 1 diabetes.
简介
高血糖导致微血管病和神经病变的生化机制尚不清楚。实验研究已经证实，患有神经病变的糖尿病啮齿动物存在氧化应激，抗氧化治疗具有保护作用。氧化应激也存在于人类糖尿病中，但它的临床重要性尚不确定。
材料与方法
我们在一项为期 3 年的纵向研究中，每年对 37 例发病时间不到 2 年的 1 型糖尿病患者进行几项生化氧化应激指标的检查。我们还对躯体感觉和自主神经功能进行了全面的年度评估。共对 41 例对照者进行了研究。
结果
丙二醛排泄量，一种脂质过氧化的指标，在对照组中为 1.5μ±0.1μmol/g 肌酐，而在发病 1 年的糖尿病患者中为 2.43μ±0.3μ，在发病 2 年中为 2.39μ±0.2μ，在发病 3 年中为 1.92μ±0.15μ，与所有年份的对照组均有差异；p<0.005。对照组血清 NOx（硝酸盐和亚硝酸盐）为 34.0μ±4.9μmol/L，而在发病 1 年的糖尿病患者中为 52.4μ±5μ，在发病 2 年中为 50.0μ±5.1μ，在发病 3 年中为 49.0μ±5.2μ，与对照组不同；p<0.01。我们测量了出汗功能，发现血糖控制不佳的糖尿病患者上半身出汗较多，下半身出汗较少，这是交感神经损伤的典型表现。上半身与下半身的出汗比为 0.385μ±0.04μ，在发病 1 年的糖尿病患者中为 0.70μ±0.14μ，在发病 2 年中为 0.51μ±0.14μ，在发病 3 年中为 0.496μ±0.12μ（与对照组不同；p<0.01，所有年份均有差异）。尿 MDA 与总汗量呈负相关（r=-39，p<0.01）；NOx 也与总汗量呈负相关（r=-0.34，p<0.025）。在早期 1 型糖尿病中，肾素（肾素/前肾素比）处理异常，这是一种肾交感神经元的检测方法。
结论
氧化应激和血清中过多的 NOx 与早期 1 型糖尿病的交感神经功能障碍有关。
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