| Bivariate linkage between acylation-stimulating protein and BMI and high-density lipoproteins. | |
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MedLine Citation:
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PMID: 15090635 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: Given the importance of visceral adiposity in the metabolic syndrome, whether levels of adipokines have shared genetic effects (pleiotropy) with aspects of the metabolic syndrome should be addressed. Acylation-stimulating protein (ASP), an adipose-derived protein, influences lipid metabolism, obesity, and glucose use. Therefore, our objective was to examine the genetic regulation of ASP and associated pleiotropic effects. RESEARCH METHODS AND PROCEDURES: We assayed serum ASP levels in 435 Mexican Americans participating in the San Antonio Family Heart Study and performed univariate and bivariate variance components analysis. RESULTS: Additive genetic heritability of ASP was 26% (p = 0.0004). Bivariate genetic analysis detected significant genetic correlations between ASP and several lipid measures but not between ASP and adiposity or diabetes measures. We detected two potential quantitative trait loci influencing ASP levels. The strongest signal was on chromosome 17 near marker D17S1303 [log of the odds ratio (LOD) = 2.7]. The signal on chromosome 15 reached its peak near marker D15S641 (LOD = 2.1). Both signals localize in regions reported to harbor quantitative trait loci influencing obesity and lipid phenotypes in this population. Bivariate linkage analysis yielded LODs of 4.7 for ASP and BMI on chromosome 17 and 3.2 for ASP and high-density lipoprotein2a on chromosome 15. DISCUSSION: Given these findings, there seems to be a significant genetic contribution to variation in circulating levels of ASP and an interesting pattern of genetic correlation (i.e., pleiotropy) with other risk factors associated with the metabolic syndrome. |
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Authors:
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Lisa J Martin; Katherine Cianflone; Robert Zakarian; Gauri Nagrani; Laura Almasy; David L Rainwater; Shelley Cole; James E Hixson; Jean W MacCluer; John Blangero; Anthony G Comuzzie |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Obesity research Volume: 12 ISSN: 1071-7323 ISO Abbreviation: Obes. Res. Publication Date: 2004 Apr |
Date Detail:
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Created Date: 2004-04-19 Completed Date: 2004-07-16 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 9305691 Medline TA: Obes Res Country: United States |
Other Details:
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Languages: eng Pagination: 669-78 Citation Subset: IM |
Affiliation:
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Southwest Foundation for Biomedical Research, San Antonio, Texas, USA. lisa.martin@cchmc.org |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adolescent Adult Aged Aged, 80 and over Blood Proteins / genetics* Body Mass Index* Chromosomes, Human, Pair 15 Chromosomes, Human, Pair 17 Complement C3a* / analogs & derivatives* Female Hispanic Americans Humans Linkage (Genetics)* Lipoproteins, HDL / genetics* Lod Score Male Metabolic Syndrome X / genetics Mexico / ethnology Middle Aged Obesity / genetics Quantitative Trait Loci |
| Grant Support | |
ID/Acronym/Agency:
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HL45522/HL/NHLBI NIH HHS; MH59490/MH/NIMH NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Blood Proteins; 0/Lipoproteins, HDL; 0/complement C3a, des-Arg-(77); 80295-42-7/Complement C3a |
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