Variants in the human β1‐,β2‐ and β3‐adrenergic receptor genes are not associated with morbid obesity in children and adolescents

Tafel, Julius; Branscheid, I.; Skwarna, B.; Schlimme, M.; Morcos, Michael; Algenstaedt, Petra; Nawroth, Peter P.; Hamann, Andreas

doi:10.1111/j.1462-8902.2004.00366.x

Cited by 25 publications

(29 citation statements)

References 14 publications

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“…The present case-control study, quantitative trait analysis and meta-analysis did not provide evidence of an impact of the variant on obesity, which is consistent with previously performed case-control studies [2,[4][5][6][7][8][9]. Previous studies have suggested sex differences [16].…”

Section: Discussionsupporting

confidence: 92%

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Studies of the associations between functional β2-adrenergic receptor variants and obesity, hypertension and type 2 diabetes in 7,808 white subjects

et al. 2007

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Aims/hypothesis Functional and common Arg16Gly and Gln27Glu polymorphisms have been identified in ADRB2, the gene encoding the β 2 -adrenergic receptor. These variants have previously been examined for association with obesity, hypertension and diabetes with inconclusive results. Materials and methods We investigated both of these variants in 7,808 unrelated, middle-aged white people for their association with obesity in a case-control study, quantitative trait analysis and meta-analysis. Moreover, both variants were investigated for their potential influence on measures of hypertension and type 2 diabetes by casecontrol and quantitative trait analyses. Results The present study did not find consistent evidence for an association of these β 2 -adrenergic receptor variants with obesity or hypertension; neither did the quantitative trait analyses show any effect of the variants on obesityrelated traits. However, both the Gly allele of the Arg16Gly variant and the Glu allele of the Gln27Glu variant showed nominal association with systolic blood pressure. Furthermore, there was a nominal association of the Arg16 allele frequency and genotype distribution with type 2 diabetes; however, no influence on quantitative biochemical phenotypes related to type 2 diabetes was found. A nominal association of the Arg/Gly genotype with the metabolic syndrome was also observed (p=0.003). Logistic regression analyses provided no evidence of a synergistic or an additive effect of these variants on obesity, hypertension or diabetes. Conclusions/interpretation After studying 7,808 middleaged white subjects, we were unable to demonstrate any consistent associations between two common amino acid polymorphisms of the β 2 -adrenergic receptor and obesity, hypertension or type 2 diabetes.

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Section: Discussionsupporting

confidence: 92%

“…Several of these failed to identify any association [3][4][5][6][7][8][9]. Other studies have found significant associations [8,10,11], but without a consensus regarding which allele is associated with obesity or related traits.…”

Section: Introductionmentioning

confidence: 99%

Studies of the associations between functional β2-adrenergic receptor variants and obesity, hypertension and type 2 diabetes in 7,808 white subjects

et al. 2007

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“…Additionally, there is some evidence to suggest that polymorphisms on the beta-2 adrenergic receptor, expressed mainly in subcutaneous adipose tissue, may also be linked to variation in BMI and obesity related phenotypes. Thus, the Arg16Glyn variant of ADRB2 has been associated with signifi cant weight gain in childhood through to young adults (Angeli et al, 2011;Ellsworth et al, 2002;Lagou et al, 2011) though data are mixed Tafel et al, 2004). This variant appears to act synergistically with the LEPR Gln223Arg SNP for risk of obesity (Angeli et al, 2011) and may moderate (ameliorate) the effect on adiposity by increased vigorous activity .…”

Section: Adrenergic Receptor Gene Variants -A Role In Polygenic Obesimentioning

confidence: 99%

Obesity and eating behaviour in children and adolescents: Contribution of common gene polymorphisms

Cecil

Dalton

Finlayson

et al. 2012

International Review of Psychiatry

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The prevalence of childhood obesity is increasing in many countries and confers risks for early type 2 diabetes, cardiovascular disease and metabolic syndrome. In the presence of potent ' obesogenic ' environments not all children become obese, indicating the presence of susceptibility and resistance. Taking an energy balance approach, susceptibility could be mediated through a failure of appetite regulation leading to increased energy intake or via diminished energy expenditure. Evidence shows that heritability estimates for BMI and body fat are paralleled by similar coeffi cients for energy intake and preferences for dietary fat. Twin studies implicate weak satiety and enhanced food responsiveness as factors determining an increase in BMI. Single gene mutations, for example in the leptin receptor gene, that lead to extreme obesity appear to operate through appetite regulating mechanisms and the phenotypic response involves overconsumption and a failure to inhibit eating. Investigations of robustly characterized common gene variants of fat mass and obesity associated ( FTO ), peroxisome proliferator-activated receptor ( PPARG ) and melanocortin 4 receptor ( MC4R ) which contribute to variance in BMI also infl uence the variance in appetite factors such as measured energy intake, satiety responsiveness and the intake of palatable energy-dense food. A review of the evidence suggests that susceptibility to childhood obesity involving specifi c allelic variants of certain genes is mediated primarily through food consumption (appetite regulation) rather than through a decrease in activity-related energy expenditure. This conclusion has implications for early detection of susceptibility, and for prevention and management of childhood obesity.

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“…2,6,7 Two candidate genes, lipoprotein lipase (LPL) gene and b1-adrenergic receptor (ADRB1) gene are considered potentially important to obesity. [8][9][10][11][12][13][14][15][16] Lipoprotein lipase as a lypolytic enzyme plays an important role in catabolism of triglycerides of chylomicrons and very low-density lipoproteins and deposition of fatty acids in adipose tissue. 17 The Ser447Stop polymorphism of LPL gene located in exon 9 produces a truncated protein without Ser-Gly dipeptide in the COOHterminus that has been associated with a favorable lipid profile.…”

mentioning

confidence: 99%

“…21,22 However, this polymorphism alone has not been associated with obesity. [14][15][16] Since adrenoreceptors and LPL are involved in pathways of lipid and energy metabolism, it has been suggested that interactions between these genes could have effect on obesity. 9,12 However, there is a paucity of information regarding the interaction effect between Ser447Stop variant of the LPL gene and Arg389Gly variant of the ADRB1 gene on obesity, especially on the development of obesity from childhood to adulthood.…”

mentioning

confidence: 99%

Influence of lipoprotein lipase gene Ser447Stop and β1-adrenergic receptor gene Arg389Gly polymorphisms and their interaction on obesity from childhood to adulthood: the Bogalusa Heart Study

Chen

Srinivasan

et al. 2006

Int J Obes

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Objective: To investigate the influence of lipoprotein lipase (LPL) Ser447Stop and b 1 -adrenergic receptor (ADRB1) Arg389Gly gene polymorphisms, individually and in combination, on obesity from childhood to adulthood. Design and subjects: A community-based cohort of 1331 subjects (30% black and 70% white subjects) was followed over an average period of 23 years from childhood (age range: 4-17 years) to adulthood (age range:18-44 years). Measurement: Body mass index (BMI, kg/m 2 ) and LPL Ser447Stop and the ADRB1 Arg389Gly genotypes. Results: The frequency of the ADRB1 Gly389 allele was 0.25 in white subjects vs 0.39 in black subjects (Po0.001); 0.08 vs 0.05 (P ¼ 0.280) for the LPL Stop447 allele. There was no association between the LPL Stop447 allele and BMI among white and black subjects either in childhood and adulthood levels or annual change from childhood to adulthood. The ADRB1 Gly389 allele was associated with lower BMI only in black adults (P ¼ 0.017). Further, the interaction effect of the LPL Stop447 allele and ADRB1 Gly389 allele on adult BMI or its annual change was significant in white subjects and in the total sample (P ¼ 0.03-0.006). Childhood values tended to show a similar trend. Having both ADRB1 Gly389 allele and LPL Stop447 allele was associated with 71% (95% confidence interval: 26-89%) less odds for developing obesity from childhood to adulthood after adjusting for age, race, sex, and childhood BMI. Conclusion: While Gly389 allele of the ADRB1 gene lowers obesity in black subjects, this allele in conjunction with Stop447 allele of the LPL gene lowers obesity in adults and attenuates the development of obesity from childhood to adulthood. These findings underscore the importance of gene-gene interaction in the assessment of genetic influences on complex traits such as obesity.

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Variants in the human β₁‐_,β₂‐ and β₃‐adrenergic receptor genes are not associated with morbid obesity in children and adolescents

Cited by 25 publications

References 14 publications

Studies of the associations between functional β2-adrenergic receptor variants and obesity, hypertension and type 2 diabetes in 7,808 white subjects

Studies of the associations between functional β2-adrenergic receptor variants and obesity, hypertension and type 2 diabetes in 7,808 white subjects

Obesity and eating behaviour in children and adolescents: Contribution of common gene polymorphisms

Influence of lipoprotein lipase gene Ser447Stop and β1-adrenergic receptor gene Arg389Gly polymorphisms and their interaction on obesity from childhood to adulthood: the Bogalusa Heart Study

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