Relationships between glucose excursion and the activation of oxidative stress in patients with newly diagnosed type 2 diabetes or impaired glucose regulation

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• 作者：Fenping Zheng (1)
  Weina Lu (1)
  Chengfang Jia (1)
  Hong Li (1)
  Zhou Wang (1)
  Weiping Jia (2)
  
• 关键词：Glucose excursion ; Oxidative stress ; Diabetes ; Impaired glucose regulation
• 刊名：Endocrine
• 出版年：2010
• 出版时间：February 2010
• 年：2010
• 卷：37
• 期：1
• 页码：201-208
• 全文大小：291KB
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• 作者单位：Fenping Zheng (1)
  Weina Lu (1)
  Chengfang Jia (1)
  Hong Li (1)
  Zhou Wang (1)
  Weiping Jia (2)
  
  1. Department of Endocrinology, The Affiliated Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, 3 East Qingchun Road, Hangzhou, 310016, China
  2. Department of Endocrinology and Metabolism, Shanghai Diabetes Institute, Sixth People’s Hospital, Jiaotong University, Shanghai, China
  

文摘

The effect of glucose excursions on oxidative stress is an important topic in diabetes research. We investigated this relationship by analyzing markers of oxidative stress and glycemic data from a continuous glucose monitoring system (CGMS) in 30 individuals with normal glucose regulation (NGR), 27 subjects with impaired glucose regulation (IGR), and 27 patients with newly diagnosed type 2 diabetes (T2DM). We compared the mean amplitude of glycemic excursion (MAGE), mean postprandial glucose excursion (MPPGE), and mean postprandial incremental area under the curve (IAUC) with plasma levels of oxidative stress markers 8-iso-PGF2α, 8-OH-dG, and protein carbonyl content in the study subjects. Patients with T2DM or IGR had significantly higher glucose excursions and plasma levels of oxidative stress markers compared to normal controls (P?<?0.01 or 0.05). Multiple linear regression analyses showed significant relationships between MAGE and plasma 8-iso-PGF2α, and between MPPGE and plasma 8-OH-dG in patients with IGR or T2DM (P?<?0.01 or 0.05). Furthermore, 2h-postprandial glucose level and IAUC were related to plasma protein carbonyl content in the study cohort including T2DM and IGR (P?<?0.01). We demonstrate that glucose excursions in subjects with IGR and T2DM trigger the activation of oxidative stress.