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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Apolipoprotein e4 allele and endothelium-dependent arterial dilation in Type 2 diabetes mellitus without angiopathy.

AIMS/HYPOTHESIS: Several studies have suggested a predisposing role of the e4 allele of apolipoprotein E (ApoE) in the development of atherosclerosis and cardiovascular disease in Type 2 diabetes. Therefore, we hypothesized that the e4 allele is also a risk factor for endothelial dysfunction. We attempted to assess whether Apo e4 allele is associated with endothelial dysfunction in the early stage of Type 2 diabetes. METHODS: We selected 255 Chinese Han Type 2 diabtetic men without angiopathy. PCR or allele-specific oligonucleotide probes were used to analyse ApoE genotypes, and high resolution ultrasound was used to measure brachial artery diameter at rest, after reactive hyperaemia and after sublingual glyceryltrinitrate. RESULTS: The flow-mediated arterial dilation among the subjects with e4/3 or e4/4 was 3.14+/-0.32%, which was lower than that in subjects with e2/2 or e3/2 (4.04+/-0.30%) ( p=0.038). The baseline vessel size, glyceryltrinitrate-induced arterial dilation and baseline flow were not different among different ApoE genotypes. On univariate analysis, reduced flow-mediated arterial dilation was related to total cholesterol, LDL, lipoprotein(a) [Lp(a)], high blood pressure, older age, family history of premature vascular disease, larger vessel size, cigarette smoking, duration of diabetes and e4 allele ( p<0.05). By multiple stepwise regression analysis, reduced flow-mediated arterial dilation was associated with cigarette smoking, LDL, Lp(a), and e4 allele ( p<0.01). CONCLUSION/INTERPRETATION: Apo e4 allele is associated with impairment of endothelium-dependent arterial dilation in the early stage of Type 2 diabetes.[1]

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