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Variants in the human β 1 ‐ , β 2 ‐ and β 3 ‐adrenergic receptor genes are not associated with morbid obesity in children and adolescents
Author(s) -
Tafel J.,
Branscheid I.,
Skwarna B.,
Schlimme M.,
Morcos M.,
Algenstaedt P.,
Hinney A.,
Hebebrand J.,
Nawroth P.,
Hamann A.
Publication year - 2004
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/j.1462-8902.2004.00366.x
Subject(s) - medicine , endocrinology , allele , genotype , allele frequency , adrenergic receptor , obesity , adrenergic , receptor , gene , thermogenesis , genetics , biology
Aim: β‐adrenergic receptors (β‐ARs) are of key importance for the regulation of lipolysis and thermogenesis by catecholamines. Genetic defects in expression or function of β 1 ‐ β 2 ‐ and/or β 3 ‐AR could affect energy homeostasis and predispose an individual towards the development of obesity. We therefore investigated the possible association of polymorphisms in the β‐adrenergic receptor genes with early onset obesity. Methods: Frequencies of the following variants were assessed in extremely obese children and healthy underweight controls: Gly/Ser in codon 49 and Arg/Gly in codon 389 of the β 1 ‐AR, Arg/Gly in codon 16 and Gln/Glu in codon 27 of the β 2 ‐AR, Trp/Arg in codon 64 of the β 3 ‐AR. Results: The Ser49 allele in the β 1 ‐AR gene was found at a frequency of 0.131 in obese and 0.136 in lean subjects (p = 0.835), while the Gly389 allele in the β 1 ‐AR had a frequency of 0.319 in obese and 0.328 in lean subjects (p = 0.802). Gly16 in the β 2 ‐AR was found with a frequency of 0.590 in obese and 0.611 in lean subjects (p = 0.591) and the Glu27 allele in the β 2 ‐AR had a frequency of 0.380 in obese and 0.420 in lean subjects (p = 0.298). Conclusion: We did not detect significant differences for allele and carrier frequencies of individual polymorphisms. Together with previously obtained data on genotype distribution of a β 3 ‐AR variant in the same study group, no significant differences were found between obese and lean subjects for the distribution of individuals with variants in none, one, two or all three β‐ARs. Our data make it unlikely that polymorphisms in β‐ARs are involved in the pathogenesis of early onset obesity.