Parham Mahmoud, Amini Massoud, Aminorroaya Ashraf, Heidarian Esfandiar
Isfahan Endocrine and Metabolism Research Center, Sedigheh Tahereh Research Complex, Isfahan University of Medical Sciences, Isfahan, Iran.
Rev Diabet Stud. 2008 Summer;5(2):102-9. doi: 10.1900/RDS.2008.5.102. Epub 2008 Aug 10.
Oxidative stress can contribute to microvascular complications in diabetes. A decisive event associated with this condition may be the decrease in the synthesis of zinc-containing antioxidant enzymes such as superoxide dismutase and glutathione peroxidase. This consideration led us to investigate the effect of zinc supplementation versus placebo on microalbuminuria in diabetic patients in a randomized double blind clinical trial.
Fifty diabetic patients with microalbuminuria were enrolled. Fasting plasma glucose, HbA1c, lipid profiles, plasma zinc levels and random urine for albumin and creatinine were measured. Patients randomly received 30 mg elemental zinc (group 1) or placebo (group 2) for 3 months. After a 4 week wash-out period, the groups were crossed over (i.e. the zinc group were given placebo, and the placebo group were given zinc) and the protocol was repeated.
From an initial number of 50 selected patients (25 in each of two groups), 39 patients (21 in group 1 and 18 in group 2) completed the study. In group 1, after zinc supplementation, urinary albumin excretion decreased significantly from 86.5 +/- 57 to 75 +/- 71 mg/g (p = 0.01). After placebo, patients in group 1 showed no significant reduction in microalbuminuria (85 +/- 72 mg/g to 83 +/- 63 mg/g creatinine). In group 2, no change in albumin excretion was observed after placebo treatment (90.5 +/- 63 mg/g to 90 +/- 60 mg/g creatinine). After zinc supplementation, a significant reduction was observed in albumin excretion, from 90 +/- 60 mg/g to 85 +/- 57 mg/g creatinine (p = 0.003).
Zinc supplementation reduced albumin excretion in microalbuminuric type 2diabetic patients. This outcome may be due to the antioxidant effect of zinc.
氧化应激可导致糖尿病微血管并发症。与这种情况相关的一个决定性事件可能是含锌抗氧化酶(如超氧化物歧化酶和谷胱甘肽过氧化物酶)合成减少。基于这一考虑,我们在一项随机双盲临床试验中研究了补充锌与安慰剂对糖尿病患者微量白蛋白尿的影响。
招募了50例患有微量白蛋白尿的糖尿病患者。测量空腹血糖、糖化血红蛋白、血脂谱、血浆锌水平以及随机尿白蛋白和肌酐。患者随机接受30毫克元素锌(第1组)或安慰剂(第2组),为期3个月。经过4周的洗脱期后,两组进行交叉(即锌组给予安慰剂,安慰剂组给予锌),并重复该方案。
从最初选择的50例患者(两组各25例)中,39例患者(第1组21例,第2组18例)完成了研究。在第1组中,补充锌后,尿白蛋白排泄量从86.5±57显著降至75±71毫克/克(p = 0.01)。服用安慰剂后,第1组患者的微量白蛋白尿无显著降低(从85±72毫克/克降至83±63毫克/克肌酐)。在第2组中,安慰剂治疗后白蛋白排泄量无变化(从90.5±63毫克/克降至90±60毫克/克肌酐)。补充锌后,白蛋白排泄量显著降低,从90±60毫克/克降至85±57毫克/克肌酐(p = 0.003)。
补充锌可降低微量白蛋白尿型2型糖尿病患者的白蛋白排泄量。这一结果可能归因于锌的抗氧化作用。