Increased plasma methylglyoxal level, inflammation, and vascular endothelial dysfunction in diabetic nephropathy

被引:116
作者
Lu, Jianxin [1 ,2 ]
Randell, Edward [3 ,4 ]
Han, YingChun [4 ]
Adeli, Khosrow [5 ]
Krahn, John [1 ]
Meng, Qing H. [1 ,2 ]
机构
[1] Univ Saskatchewan, Dept Pathol & Lab Med, Royal Univ Hosp, Saskatoon, SK S7N 0W8, Canada
[2] Wenzhou Med Coll, Sch Lab Med, Zhejiang Prov Key Lab Med Genet, Key Lab Lab Med,Minist Educ, Wenzhou, Peoples R China
[3] Mem Univ Newfoundland, Fac Med, Dept Basic Sci, St John, NF, Canada
[4] Mem Univ Newfoundland, Fac Med, Div Lab Med, St John, NF, Canada
[5] Univ Toronto, Dept Pathobiol & Lab Med, Toronto, ON, Canada
关键词
Methylglyoxal; Cytokines; Adhesion molecules; Diabetes; Diabetic; Nephropathy; COMPLICATION-FREE PATIENTS; GLYCATION END-PRODUCTS; NECROSIS-FACTOR-ALPHA; DIETARY GLYCOTOXINS; GLYCEMIC CONTROL; MARKERS; MECHANISM; MELLITUS; RISK; MICROALBUMINURIA;
D O I
10.1016/j.clinbiochem.2010.11.004
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Objectives: To investigate the association of plasma levels of methylglyoxal (MG) and markers of inflammation/endothelial dysfunction with diabetic nephropathy (DN). Design and methods: Plasma levels of MG, cytokines, and adhesion molecules were measured in type 2 diabetic patients (T2DM), T2DM patients with DN, and the controls. Results: Plasma MG levels in DN were significantly higher than those in T2DM and the controls (312 +/- 135 vs. 212 +/- 73 and 312 +/- 135 vs. 147 +/- 78 nmol/L, respectively, P < 0.001). The plasma levels of MG were positively correlated with the fasting glucose, HbA1c, and urinary albumin/creatinine ratio (r = 0.754. P < 0.05). Plasma levels of IL-6, TNF-alpha, and adhesion molecules were markedly increased in DN compared to T2DM patients and the controls. Conclusions: Increased plasma levels of MG, cytokines, and adhesion molecules are associated with DN. These markers may be useful in predicting the development of DN. (C) 2010 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:307 / 311
页数:5
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