Acharya Jhankar D, Pande Amol J, Joshi Suyog M, Yajnik Chittaranjan S, Ghaskadbi Saroj S
Department of Zoology, University of Pune, Pune, 411 007, India.
Diabetes Metab Res Rev. 2014 Oct;30(7):590-8. doi: 10.1002/dmrr.2526.
There exist several reports demonstrating enhancement in oxidative stress in diabetic patients; however, serial and comprehensive measurement of oxidative stress parameters in newly diagnosed diabetic patients is not yet reported. We measured the oxidative stress parameters in diabetic patients serially from the time of diagnosis and after starting treatment to study their association with glycaemia, insulin resistance and β-cell function.
Fifty-four newly diagnosed diabetic patients were studied at diagnosis and 4 and 8 weeks after initiating anti-hyperglycaemic treatment. Oxidative stress parameters included activity of antioxidant enzymes, concentration of antioxidant molecules and damage markers. Oxidative stress score was computed as a collective measure of oxidative stress to interpret total oxidative stress state. Association of changing glucose levels with changing oxidative stress parameters over 8 weeks and association of oxidative stress score with insulin resistance and β-cell function was analysed by homeostasis model assessment (HOMA-IR and HOMA-β, respectively).
Eight weeks of treatment improved HbA1C from 9.8 ± 2.1 to 7.7 ± 1.0%. There was a significant increase in oxidative stress in diabetic patients [23.8 (95% CI 20.0, 27.6)] compared with non-diabetic subjects [-1.2 (-3.4, 0.9)] (p < 0.001). Non-diabetic subjects showed a stable status over 8 weeks. Improvement in hyperglycaemia in diabetic patients was associated with an improvement in oxidative stress parameters irrespective of the anti-diabetic treatment received. Oxidative stress score fell after 8 weeks and was significantly associated with an improvement in HOMA-β (standardized β = -0.38, p < 0.01) but not with HOMA-IR.
Controlling hyperglycaemia in diabetic patients alleviates oxidative stress within 8 weeks of treatment, and improvement in oxidative stress parameters was related to an improved β-cell function.
已有多项报告表明糖尿病患者的氧化应激增强；然而，尚未有关于新诊断糖尿病患者氧化应激参数的系列和综合测量的报道。我们从诊断时起并在开始治疗后对糖尿病患者的氧化应激参数进行了连续测量，以研究它们与血糖、胰岛素抵抗和β细胞功能的关系。
对54例新诊断的糖尿病患者在诊断时以及开始抗高血糖治疗后的4周和8周进行了研究。氧化应激参数包括抗氧化酶活性、抗氧化分子浓度和损伤标志物。计算氧化应激评分作为氧化应激的综合指标，以解释总的氧化应激状态。通过稳态模型评估（分别为HOMA-IR和HOMA-β）分析8周内血糖水平变化与氧化应激参数变化的关系以及氧化应激评分与胰岛素抵抗和β细胞功能的关系。
治疗8周后，糖化血红蛋白（HbA1C）从9.8±2.1%改善至7.7±1.0%。与非糖尿病受试者[-1.2（-3.4，0.9）]相比，糖尿病患者的氧化应激显著增加[23.8（95%可信区间20.0，27.6）]（p<0.001）。非糖尿病受试者在8周内表现出稳定状态。无论接受何种抗糖尿病治疗，糖尿病患者高血糖的改善都与氧化应激参数的改善相关。8周后氧化应激评分下降，且与HOMA-β的改善显著相关（标准化β=-0.38，p<0.01），但与HOMA-IR无关。
控制糖尿病患者的高血糖在治疗8周内可减轻氧化应激，氧化应激参数的改善与β细胞功能的改善有关。
