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

Endocrine

Department of Endocrinology and Metabolism, Hangzhou Hospital, Nanjing Medical University, Xueshi Road 4#, Hangzhou City, Zhejiang Province, 310006, China.

Published: August 2011

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).

Download full-text PDF

Source
http://dx.doi.org/10.1007/s12020-011-9442-9DOI Listing

Publication Analysis

Top Keywords

il-6 gene
20
gene promoter
20
endothelial dysfunction
8
promoter -174g/c
8
-174g/c -572g/c
8
-572g/c polymorphism
8
endothelial function
8
ngr subjects
8
t2dm patients
8
promoter region
8

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!