Heid, Iris M. and Henneman, Peter and Hicks, Andrew and Coassin, Stefan and Winkler, Thomas and Aulchenko, Yurii S. and Fuchsberger, Christian and Song, Kijoung and Hivert, Marie-France and Waterworth, Dawn M. and Timpson, Nicholas J. and Richards, J. Brent and Perry, John R. B. and Tanaka, Toshiko and Amin, Najaf and Kollerits, Barbara and Pichler, Irene and Oostra, Ben A. and Thorand, Barbara and Frants, Rune R. and Illig, Thomas and Dupuis, Josee and Glaser, Beate and Spector, Tim and Guralnik, Jack and Egan, Josephine M. and Florez, Jose C. and Evans, David M. and Soranzo, Nicole and Bandinelli, Stefania and Carlson, Olga D. and Frayling, Timothy M. and Burling, Keith and Smith, George Davey and Mooser, Vincent and Ferrucci, Luigi and Meigs, James B. and Vollenweider, Peter and van Dijk, Ko Willems and Pramstaller, Peter and Kronenberg, Florian and van Duijn, Cornelia M. (2010) Clear detection of ADIPOQ locus as the major gene for plasma adiponectin: Results of genome-wide association analyses including 4659 European individuals. ATHEROSCLEROSIS, 208 (2). pp. 412-420. ISSN 0021-9150, 1879-1484
Full text not available from this repository. (Request a copy)Abstract
Objective: Plasma adiponectin is strongly associated with various components of metabolic syndrome, type 2 diabetes and cardiovascular outcomes. Concentrations are highly heritable and differ between men and women. We therefore aimed to investigate the genetics of plasma adiponectin in men and women. Methods: Wecombined genome-wide association scans of three population-based studies including 4659 persons. For the replication stage in 13795 subjects, we selected the 20 top signals of the combined analysis, as well as the 10 top signals with p-values less than 1.0 x 10(-4) for each the men-and the women-specific analyses. We further selected 73 SNPs that were consistently associated with metabolic syndrome parameters in previous genome-wide association studies to check for their association with plasma adiponectin. Results: The ADIPOQ locus showed genome-wide significant p-values in the combined (p = 4.3 x 10(-24)) as well as in both women-and men-specific analyses (p = 8.7 x 10(-17) and p = 2.5 x 10(-11), respectively). None of the other 39 top signal SNPs showed evidence for association in the replication analysis. None of 73 SNPs from metabolic syndrome loci e x hibited association with plasma adiponectin (p > 0.01). Conclusions: We demonstrated the ADIPOQ gene as the only major gene for plasma adiponectin, which e x plains 6.7% of the phenotypic variance. We further found that neither this gene nor any of the metabolic syndrome loci e x plained the se x differences observed for plasma adiponectin. Larger studies are needed to identify more moderate genetic determinants of plasma adiponectin. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | METABOLIC SYNDROME; INSULIN-RESISTANCE; APM1 GENE; RISK; PROMOTER; DISEASE; OBESITY; PREVALENCE; CAUCASIANS; CONTRIBUTE; Adiponectin; Genome-wide association study; Polymorphism; Cardiovascular disease; Metabolic syndrome |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Institut für Epidemiologie und Präventivmedizin |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 07 Aug 2020 09:26 |
| Last Modified: | 07 Aug 2020 09:26 |
| URI: | https://pred.uni-regensburg.de/id/eprint/25173 |
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