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Erschienen in: Endocrine 1/2011

01.08.2011 | Original Article

The endothelial dysfunction in patients with type 2 diabetes mellitus is associated with IL-6 gene promoter polymorphism in Chinese population

verfasst von: Xianfeng Zhang, Lizhen Ma, Fengying Peng, Yin Wu, Yu Chen, Linying Yu, Zhikai Lei, Chu Zhang

Erschienen in: Endocrine | Ausgabe 1/2011

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Abstract

The purpose of this study is to examine the effects of IL-6 gene promoter −174G/C and −572G/C polymorphism on endothelial function of Chinese T2DM and normal glucose regulation (NGR) subjects. 512 newly diagnosed T2DM patients and 483 NGR subjects were recruited and Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) was performed for the IL-6 gene promoter −174G/C and −572G/C polymorphism. Flow-mediated dilation (FMD) was measured as a non-invasive indicator for endothelial function. The results show that the C allele and CC genotype at −174 of IL-6 gene promoter region was extremely rare in both T2DM and NGR groups; genotypes’ and alleles’ frequency at −572 of IL-6 gene promoter region is of no difference between T2DM and NGR groups; within T2DM group, higher plasma IL-6 concentration and lower FMD was found in patients with −572 GC (2.36 ± 0.69, 4.23 ± 3.82%) or GG (2.32 ± 0.74, 4.24 ± 3.67%) genotype, compared with patients with CC (2.15 ± 0.62, 5.28 ± 3.94%) genotype. The conclusion of the study is that in comparison with patients of CC genotype, the T2DM patients of −572 GC or GG genotype may have more aggravated endothelial dysfunction (ED) and be at higher risk for coronary artery disease (CAD).
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Metadaten
Titel
The endothelial dysfunction in patients with type 2 diabetes mellitus is associated with IL-6 gene promoter polymorphism in Chinese population
verfasst von
Xianfeng Zhang
Lizhen Ma
Fengying Peng
Yin Wu
Yu Chen
Linying Yu
Zhikai Lei
Chu Zhang
Publikationsdatum
01.08.2011
Verlag
Springer US
Erschienen in
Endocrine / Ausgabe 1/2011
Print ISSN: 1355-008X
Elektronische ISSN: 1559-0100
DOI
https://doi.org/10.1007/s12020-011-9442-9

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