Studies of the association of the GNB3 825C&gt;T polymorphism with components of the metabolic syndrome in white Danes

Andersen, Gitte; Overgaard, Jesper; Albrechtsen, Anders; Glümer, Charlotte; Borch‐Johnsen, Knut; Jørgensen, Torben; Hansen, Torben; Pedersen, Oluf

doi:10.1007/s00125-005-0049-7

Cited by 41 publications

(35 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this study, single locus analyses did not show significant main effects of GNB3 rs5443 (in either genotypic test or odds ratio analysis) on the risk of obesity or overweight in the subjects. Our results were in agreement with those of several other studies (Andersen et al 2006;Hayakawa et al 2007;Suwazono et al 2004). A previous study by Andersen et al (2006) suggested that there is no major involvement of the GNB3 rs5443 polymorphism in obesity in white Danish subjects.…”

Section: Discussionsupporting

confidence: 94%

“…Our results were in agreement with those of several other studies (Andersen et al 2006;Hayakawa et al 2007;Suwazono et al 2004). A previous study by Andersen et al (2006) suggested that there is no major involvement of the GNB3 rs5443 polymorphism in obesity in white Danish subjects. Hayakawa et al (2007) also demonstrated that the GNB3 rs5443 polymorphism is unlikely to influence obesity in Japanese subjects who underwent general health examinations.…”

Section: Discussionsupporting

confidence: 94%

“…Hayakawa et al (2007) also found that GNB3 rs5443 was not associated with triglyceride. Possible explanations for the discrepancies in these studies may be the use of insufficient sample sizes, varied phenotype assessment, differences in ethnicity, different study designs, and a lack of adjustment for confounding effects (Andersen et al 2006). The GNB3 rs5443 polymorphism has been widely implicated in affecting obesity risk, although genetic evidence of its effect on obesity has been inconsistent.…”

Section: Discussionmentioning

confidence: 99%

“…The T allele of GNB3 rs5443 SNP has been reported to predispose to obesity in German (Brand et al 2003;Siffert et al 1999;Stefan et al 2004), Chinese (Siffert et al 1999), and South African (Siffert et al 1999) populations. On the contrary, this association with obesity has not been replicated in white Danish subjects (Andersen et al 2006) and in a Japanese study (Hayakawa et al 2007). In addition, data from a study support the notion that there was statistically significant association of this SNP with total cholesterol levels in a Japanese population (indicating higher in subjects with the T allele) (Ishikawa et al 2000), even though there are some conflicting results in another Japanese study showing no association with cholesterol (Suwazono et al 2006).…”

Section: Introductionmentioning

confidence: 93%

See 3 more Smart Citations

Association of the C825T polymorphism in the GNB3 gene with obesity and metabolic phenotypes in a Taiwanese population

et al. 2012

View full text Add to dashboard Cite

The relationship between obesity and a single nucleotide polymorphism (SNP), rs5443 (C825T), in the guanine nucleotide binding protein beta polypeptide 3 (GNB3) gene is currently inconsistent. In this study, we aimed to reassess whether the GNB3 rs5443 SNP could influence obesity and obesity-related metabolic traits in a Taiwanese population. A total of 983 Taiwanese subjects with general health examinations were genotyped. Based on the criteria defined by the Department of Health in Taiwan, the terms ''overweight'' and ''obesity'' are defined as 24 2 BMI \ 27 and BMI 3 27, respectively. Compared to the carrier of the combined CT ? TT genotypes of the GNB3 rs5443 polymorphism, triglyceride was significantly higher for the carrier of CC genotype in the complete sample population (128.2 ± 93.2 vs. 114.3 ± 79.1 mg/dl; P = 0.041). In addition, the carriers of CC variant had a higher total cholesterol than those with the combined CT ? TT variants (194.5 ± 36.8 vs. 187.9 ± 33.0 mg/dl; P = 0.019) in the complete sample population. In the normal controls, both triglyceride (P = 0.018) and total cholesterol (P = 0.011) were also significantly higher in the CC homozygotes than in the combined CT ? TT genotypes. However, the GNB3 rs5443 SNP did not exhibit any significant association with obesity or overweight among the subjects. Our study indicates that the CC genotype of the GNB3 rs5443 SNP may predict higher obesity-related metabolic traits such as triglyceride and total cholesterol in non-obese Taiwanese subjects (but not in obese subjects).

show abstract

Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 93%

See 2 more Smart Citations

Association of the C825T polymorphism in the GNB3 gene with obesity and metabolic phenotypes in a Taiwanese population

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Biochemical, anthropometric and physiological measurements These analyses were performed as previously described [22].…”

Section: Subjects and Materialsmentioning

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

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Molecular Genetics of Metabolic Syndrome

Chang

Chuang

2013

Encyclopedia of Life Sciences

View full text Add to dashboard Cite

The clustering of metabolic traits (known as metabolic syndrome), including central obesity, abnormal glucose regulation, dyslipidemia and elevated blood pressure, was associated with increased risk of cardiovascular disease and type 2 diabetes. The close clustering and strong heritability of these metabolic traits suggest a common underlying genetic basis. Genetically modified mice models and identification of causative gene for human monogenic obesity/insulin resistance syndrome provided important insights into the pathogenesis of the metabolic syndrome. Recent genome‐wide association studies (GWAS) also identified several genes reproducibly associated with the metabolic syndrome or multiple metabolic traits, including genes involved in lipid metabolism ( CETP, APOA1/C3/A4/A5 cluster, LPL , LIPC and ABCB11 ), glucose sensing ( GCKR ), insulin signalling ( IRS1 ), beta‐cell function (TCF7L2) and appetite control ( FTO ). However, these variants explain only a small fraction of the observed heritability. Further pursuit for structural variants, rare sequence variants and epigenetic modification related to the metabolic syndrome may help to elucidate the unexplained heritability. Key Concepts: The estimated heritability of the metabolic syndrome and related metabolic traits (including obesity, dyslipidemia, abnormal glucose regulation and elevated blood pressure) is relatively high. Genetically modified knockout mice models and human monogenic obese/insulin resistant syndrome provide important molecular insights into the pathogenesis of the metabolic syndrome. Family linkage mapping for the metabolic syndrome is of limited success because of inconsistency among studies. Large‐scale genome‐wide association mapping identified many genetic loci associated with the metabolic syndrome and related traits. Important loci are located in genes involved in lipid metabolism ( CETP, APOA1/C3/A4/A5 cluster, LPL , LIPC and ABCB11 ), glucose sensing ( GCKR ), insulin signalling ( IRS1 ), beta‐cell function (TCF7L2) and appetite control ( FTO ). The genetic variants identified by genome‐wide association mapping explain only a minor fraction of the estimated heritability. Other potential contributors to the unexplained heritability are structural variants, rare sequence variants and epigenetic modification.

show abstract

Studies of the association of the GNB3 825C>T polymorphism with components of the metabolic syndrome in white Danes

Cited by 41 publications

References 53 publications

Association of the C825T polymorphism in the GNB3 gene with obesity and metabolic phenotypes in a Taiwanese population

Association of the C825T polymorphism in the GNB3 gene with obesity and metabolic phenotypes in a Taiwanese population

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

Molecular Genetics of Metabolic Syndrome

Contact Info

Product

Resources

About