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Studies of associations between the Arg389Gly polymorphism of the β 1 ‐adrenergic receptor gene ( ADRB1 ) and hypertension and obesity in 7677 Danish white subjects
Author(s) -
Gjesing A. P.,
Andersen G.,
Albrechtsen A.,
Glümer C.,
BorchJohnsen K.,
Jørgensen T.,
Hansen T.,
Pedersen O.
Publication year - 2007
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.2006.02031.x
Subject(s) - medicine , endocrinology , blood pressure , body mass index , allele , population , genotype , obesity , hyperinsulinemia , allele frequency , adipose tissue , insulin resistance , genetics , biology , gene , environmental health
Aims  Activation of the β 1 ‐adrenergic receptor ( ADRB1 ) causes increased lipolysis in adipose tissue and enhances cardiac output. Analysis of the association of the functional ADRB1 Arg389Gly variant with obesity and hypertension has given ambiguous results. To clarify the potential impact of this variant on obesity and hypertension in the general population, we examined the Arg389Gly variant in a relatively large‐scale population‐based study. Methods  Case‐control studies and quantitative trait analyses were carried out in 7677 Danish Caucasians who were genotyped for the Arg389Gly variant (dbSNP rs1801253) using matrix‐assisted laser desorption/ionization time‐of‐flight mass spectrometry. Results  A weak association between the Gly allele of the Arg389Gly variant and obesity was observed when comparing cases ( n  = 1540) defined as body mass index (BMI) > 30 kg/m 2 with control subjects ( n  = 6108) defined as BMI ≤ 30 kg/m 2 for both allele frequencies ( P =  0.05) and genotype distribution ( P =  0.05). Case‐control studies (cases n  = 2518; control n  = 3981) examining the effect on hypertension showed no association with allele frequencies ( P =  0.3) or genotype distribution ( P =  0.5); however, in the quantitative trait analyses, individuals carrying the Gly allele had slightly but significantly lower diastolic (Arg/Arg = 81.9 mmHg vs. Gly‐allele carriers = 81.5 mmHg) and systolic (Arg/Arg = 129.4 mmHg vs. Gly‐allele carriers = 128.8 mmHg) blood pressure as well as a lower mean arterial blood pressure. Conclusion  Our results suggest that the Arg389Gly polymorphism does not have any clinically important impact on the pathogenesis of obesity in Danish white subjects. Furthermore, despite the observed minor influence on blood pressure, this variant is most likely not to be a major contributor to the development of hypertension.

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