Cigarette smoking status has a modifying effect on the association between polymorphisms in KALRN and measures of cardiovascular risk in the diabetes heart study
All manifestations of cardiovascular disease (CVD) are substantially more common in patients with type 2 diabetes mellitus (T2DM) than in non-diabetic individuals. The current study evaluated KALRN , a gene previously linked to CVD, as a contributor to CVD in a sample enriched for T2DM. Specifically...
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| Veröffentlicht in: | Genes & genomics Jg. 33; H. 5; S. 483 - 490 |
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| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
Heidelberg
The Genetics Society of Korea
01.10.2011
한국유전학회 |
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| ISSN: | 1976-9571, 2092-9293 |
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| Abstract | All manifestations of cardiovascular disease (CVD) are substantially more common in patients with type 2 diabetes mellitus (T2DM) than in non-diabetic individuals. The current study evaluated
KALRN
, a gene previously linked to CVD, as a contributor to CVD in a sample enriched for T2DM. Specifically, the potential modifying effect of cigarette smoking was examined. A total of 28 SNPs in
KALRN
were genotyped in 1001 European Americans from 369 Diabetes Heart Study (DHS) families, as well as 762 population-based controls. The association between each SNP and both qualitative and quantitative CVD disease phenotypes was determined using generalized estimating equations and variance component models, respectively. Selected
KALRN
SNPs were found to be associated with both the qualitative (T2DM, CVD, metabolic syndrome) and quantitative traits (C-reactive protein and abdominal aortic calcified plaque). Interaction analysis and stratification were then used to test whether smoking modulates the genetic effects of
KALRN
. The strongest evidence of a modifying effect of smoking status was observed for rs9289231 and intima-media thickness (p=9.0x10
−4
) and abdominal aortic calcified plaque (p=3.0×10
−4
). Overall, following stratification by smoking status, the evidence of association with quantitative traits was more pronounced in smokers compared to non-smokers. The strongest association for smokers was between rs1720960 and abdominal aortic calcified plaque (p=2.6x10
−5
), while in non-smokers there was no observed association.
KALRN
variants are associated with measures of CVD and T2DM in the DHS sample with smoking status observed to have a significant modifying effect on these associations. |
|---|---|
| AbstractList | All manifestations of cardiovascular disease (CVD) are substantially more common in patients with type 2 diabetes mellitus (T2DM) than in non-diabetic individuals. The current study evaluated KALRN, a gene previously linked to CVD, as a contributor to CVD in a sample enriched for T2DM. Specifically,the potential modifying effect of cigarette smoking was examined. A total of 28 SNPs in KALRN were genotyped in 1001 European Americans from 369 Diabetes Heart Study (DHS) families, as well as 762 population-based controls. The association between each SNP and both qualitative and quantitative CVD disease phenotypes was determined using generalized estimating equations and variance component models,respectively. Selected KALRN SNPs were found to be associated with both the qualitative (T2DM, CVD, metabolic syndrome)and quantitative traits (C-reactive protein and abdominal aortic calcified plaque). Interaction analysis and stratification were then used to test whether smoking modulates the genetic effects of KALRN. The strongest evidence of a modifying effect of smoking status was observed for rs9289231 and intima-media thickness (p=9.0x10^(-4)) and abdominal aortic calcified plaque (p=3.0x10^(-4)). Overall, following stratification by smoking status, the evidence of association with quantitative traits was more pronounced in smokers compared to non-smokers. The strongest association for smokers was between rs1720960 and abdominal aortic calcified plaque (p=2.6x10^(-5)), while in non-smokers there was no observed association. KALRN variants are associated with measures of CVD and T2DM in the DHS sample with smoking status observed to have a significant modifying effect on these associations. KCI Citation Count: 2 All manifestations of cardiovascular disease (CVD) are substantially more common in patients with type 2 diabetes mellitus (T2DM) than in non-diabetic individuals. The current study evaluated KALRN , a gene previously linked to CVD, as a contributor to CVD in a sample enriched for T2DM. Specifically, the potential modifying effect of cigarette smoking was examined. A total of 28 SNPs in KALRN were genotyped in 1001 European Americans from 369 Diabetes Heart Study (DHS) families, as well as 762 population-based controls. The association between each SNP and both qualitative and quantitative CVD disease phenotypes was determined using generalized estimating equations and variance component models, respectively. Selected KALRN SNPs were found to be associated with both the qualitative (T2DM, CVD, metabolic syndrome) and quantitative traits (C-reactive protein and abdominal aortic calcified plaque). Interaction analysis and stratification were then used to test whether smoking modulates the genetic effects of KALRN . The strongest evidence of a modifying effect of smoking status was observed for rs9289231 and intima-media thickness (p=9.0x10 −4 ) and abdominal aortic calcified plaque (p=3.0×10 −4 ). Overall, following stratification by smoking status, the evidence of association with quantitative traits was more pronounced in smokers compared to non-smokers. The strongest association for smokers was between rs1720960 and abdominal aortic calcified plaque (p=2.6x10 −5 ), while in non-smokers there was no observed association. KALRN variants are associated with measures of CVD and T2DM in the DHS sample with smoking status observed to have a significant modifying effect on these associations. |
| Author | Langefeld, Carl D. Rudock, Megan E. Connelly, Jessica J. Horne, Benjamin D. Ziegler, Julie T. Freedman, Barry I. Cox, Amanda. J. Bowden, Donald W. Carr, J. Jeffrey Hauser, Elizabeth R. Lehtinen, Allison B. |
| Author_xml | – sequence: 1 givenname: Megan E. surname: Rudock fullname: Rudock, Megan E. organization: Center for Human Genomics, Wake Forest School of Medicine, Center for Diabetes Research, Wake Forest School of Medicine, Department of Biochemistry, Wake Forest School of Medicine – sequence: 2 givenname: Amanda. J. surname: Cox fullname: Cox, Amanda. J. organization: Center for Human Genomics, Wake Forest School of Medicine, Center for Diabetes Research, Wake Forest School of Medicine, Department of Biochemistry, Wake Forest School of Medicine – sequence: 3 givenname: Julie T. surname: Ziegler fullname: Ziegler, Julie T. organization: Department of Biostatistical Sciences, Wake Forest School of Medicine – sequence: 4 givenname: Allison B. surname: Lehtinen fullname: Lehtinen, Allison B. organization: Center for Human Genomics, Wake Forest School of Medicine, Center for Diabetes Research, Wake Forest School of Medicine, Department of Biochemistry, Wake Forest School of Medicine – sequence: 5 givenname: Jessica J. surname: Connelly fullname: Connelly, Jessica J. organization: Center for Human Genetics, School of Medicine, Duke University Medical Center – sequence: 6 givenname: Barry I. surname: Freedman fullname: Freedman, Barry I. organization: Department of Internal Medicine, Wake Forest School of Medicine – sequence: 7 givenname: J. Jeffrey surname: Carr fullname: Carr, J. Jeffrey organization: Department of Radiologic Sciences, Wake Forest School of Medicine – sequence: 8 givenname: Carl D. surname: Langefeld fullname: Langefeld, Carl D. organization: Department of Biostatistical Sciences, Wake Forest School of Medicine – sequence: 9 givenname: Elizabeth R. surname: Hauser fullname: Hauser, Elizabeth R. organization: Center for Human Genetics, School of Medicine, Duke University Medical Center – sequence: 10 givenname: Benjamin D. surname: Horne fullname: Horne, Benjamin D. organization: Cardiovascular Department, Intermountain Medical Center, University of Utah – sequence: 11 givenname: Donald W. surname: Bowden fullname: Bowden, Donald W. email: dbowden@wakehealth.edu organization: Center for Human Genomics, Wake Forest School of Medicine, Center for Diabetes Research, Wake Forest School of Medicine, Department of Biochemistry, Wake Forest School of Medicine |
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| Keywords | Type 2 diabetes Kalirin Polymorphisms Vascular Calcification |
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