Protein-Truncating Variants at the Cholesteryl Ester Transfer Protein Gene and Risk for Coronary Heart Disease
Therapies that inhibit CETP (cholesteryl ester transfer protein) have failed to demonstrate a reduction in risk for coronary heart disease (CHD). Human DNA sequence variants that truncate the gene may provide insight into the efficacy of CETP inhibition. To test whether protein-truncating variants (...
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| Published in | Circulation research Vol. 121; no. 1; pp. 81 - 88 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Lippincott Williams & Wilkins Ovid Technologies
23.06.2017
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 0009-7330 1524-4571 1524-4571 |
| DOI | 10.1161/CIRCRESAHA.117.311145 |
Cover
| Abstract | Therapies that inhibit CETP (cholesteryl ester transfer protein) have failed to demonstrate a reduction in risk for coronary heart disease (CHD). Human DNA sequence variants that truncate the
gene may provide insight into the efficacy of CETP inhibition.
To test whether protein-truncating variants (PTVs) at the
gene were associated with plasma lipid levels and CHD.
We sequenced the exons of the
gene in 58 469 participants from 12 case-control studies (18 817 CHD cases, 39 652 CHD-free controls). We defined PTV as those that lead to a premature stop, disrupt canonical splice sites, or lead to insertions/deletions that shift frame. We also genotyped 1 Japanese-specific PTV in 27561 participants from 3 case-control studies (14 286 CHD cases, 13 275 CHD-free controls). We tested association of
PTV carrier status with both plasma lipids and CHD. Among 58 469 participants with
gene-sequencing data available, average age was 51.5 years and 43% were women; 1 in 975 participants carried a PTV at the
gene. Compared with noncarriers, carriers of PTV at
had higher high-density lipoprotein cholesterol (effect size, 22.6 mg/dL; 95% confidence interval, 18-27;
<1.0×10
), lower low-density lipoprotein cholesterol (-12.2 mg/dL; 95% confidence interval, -23 to -0.98;
=0.033), and lower triglycerides (-6.3%; 95% confidence interval, -12 to -0.22;
=0.043).
PTV carrier status was associated with reduced risk for CHD (summary odds ratio, 0.70; 95% confidence interval, 0.54-0.90;
=5.1×10
).
Compared with noncarriers, carriers of PTV at
displayed higher high-density lipoprotein cholesterol, lower low-density lipoprotein cholesterol, lower triglycerides, and lower risk for CHD. |
|---|---|
| AbstractList | Therapies that inhibit CETP (cholesteryl ester transfer protein) have failed to demonstrate a reduction in risk for coronary heart disease (CHD). Human DNA sequence variants that truncate the
gene may provide insight into the efficacy of CETP inhibition.
To test whether protein-truncating variants (PTVs) at the
gene were associated with plasma lipid levels and CHD.
We sequenced the exons of the
gene in 58 469 participants from 12 case-control studies (18 817 CHD cases, 39 652 CHD-free controls). We defined PTV as those that lead to a premature stop, disrupt canonical splice sites, or lead to insertions/deletions that shift frame. We also genotyped 1 Japanese-specific PTV in 27561 participants from 3 case-control studies (14 286 CHD cases, 13 275 CHD-free controls). We tested association of
PTV carrier status with both plasma lipids and CHD. Among 58 469 participants with
gene-sequencing data available, average age was 51.5 years and 43% were women; 1 in 975 participants carried a PTV at the
gene. Compared with noncarriers, carriers of PTV at
had higher high-density lipoprotein cholesterol (effect size, 22.6 mg/dL; 95% confidence interval, 18-27;
<1.0×10
), lower low-density lipoprotein cholesterol (-12.2 mg/dL; 95% confidence interval, -23 to -0.98;
=0.033), and lower triglycerides (-6.3%; 95% confidence interval, -12 to -0.22;
=0.043).
PTV carrier status was associated with reduced risk for CHD (summary odds ratio, 0.70; 95% confidence interval, 0.54-0.90;
=5.1×10
).
Compared with noncarriers, carriers of PTV at
displayed higher high-density lipoprotein cholesterol, lower low-density lipoprotein cholesterol, lower triglycerides, and lower risk for CHD. Therapies that inhibit CETP (cholesteryl ester transfer protein) have failed to demonstrate a reduction in risk for coronary heart disease (CHD). Human DNA sequence variants that truncate the CETP gene may provide insight into the efficacy of CETP inhibition.RATIONALETherapies that inhibit CETP (cholesteryl ester transfer protein) have failed to demonstrate a reduction in risk for coronary heart disease (CHD). Human DNA sequence variants that truncate the CETP gene may provide insight into the efficacy of CETP inhibition.To test whether protein-truncating variants (PTVs) at the CETP gene were associated with plasma lipid levels and CHD.OBJECTIVETo test whether protein-truncating variants (PTVs) at the CETP gene were associated with plasma lipid levels and CHD.We sequenced the exons of the CETP gene in 58 469 participants from 12 case-control studies (18 817 CHD cases, 39 652 CHD-free controls). We defined PTV as those that lead to a premature stop, disrupt canonical splice sites, or lead to insertions/deletions that shift frame. We also genotyped 1 Japanese-specific PTV in 27561 participants from 3 case-control studies (14 286 CHD cases, 13 275 CHD-free controls). We tested association of CETP PTV carrier status with both plasma lipids and CHD. Among 58 469 participants with CETP gene-sequencing data available, average age was 51.5 years and 43% were women; 1 in 975 participants carried a PTV at the CETP gene. Compared with noncarriers, carriers of PTV at CETP had higher high-density lipoprotein cholesterol (effect size, 22.6 mg/dL; 95% confidence interval, 18-27; P<1.0×10-4), lower low-density lipoprotein cholesterol (-12.2 mg/dL; 95% confidence interval, -23 to -0.98; P=0.033), and lower triglycerides (-6.3%; 95% confidence interval, -12 to -0.22; P=0.043). CETP PTV carrier status was associated with reduced risk for CHD (summary odds ratio, 0.70; 95% confidence interval, 0.54-0.90; P=5.1×10-3).METHODS AND RESULTSWe sequenced the exons of the CETP gene in 58 469 participants from 12 case-control studies (18 817 CHD cases, 39 652 CHD-free controls). We defined PTV as those that lead to a premature stop, disrupt canonical splice sites, or lead to insertions/deletions that shift frame. We also genotyped 1 Japanese-specific PTV in 27561 participants from 3 case-control studies (14 286 CHD cases, 13 275 CHD-free controls). We tested association of CETP PTV carrier status with both plasma lipids and CHD. Among 58 469 participants with CETP gene-sequencing data available, average age was 51.5 years and 43% were women; 1 in 975 participants carried a PTV at the CETP gene. Compared with noncarriers, carriers of PTV at CETP had higher high-density lipoprotein cholesterol (effect size, 22.6 mg/dL; 95% confidence interval, 18-27; P<1.0×10-4), lower low-density lipoprotein cholesterol (-12.2 mg/dL; 95% confidence interval, -23 to -0.98; P=0.033), and lower triglycerides (-6.3%; 95% confidence interval, -12 to -0.22; P=0.043). CETP PTV carrier status was associated with reduced risk for CHD (summary odds ratio, 0.70; 95% confidence interval, 0.54-0.90; P=5.1×10-3).Compared with noncarriers, carriers of PTV at CETP displayed higher high-density lipoprotein cholesterol, lower low-density lipoprotein cholesterol, lower triglycerides, and lower risk for CHD.CONCLUSIONSCompared with noncarriers, carriers of PTV at CETP displayed higher high-density lipoprotein cholesterol, lower low-density lipoprotein cholesterol, lower triglycerides, and lower risk for CHD. Rationale:Therapies that inhibit CETP (cholesteryl ester transfer protein) have failed to demonstrate a reduction in risk for coronary heart disease (CHD). Human DNA sequence variants that truncate the CETP gene may provide insight into the efficacy of CETP inhibition.Objective:To test whether protein-truncating variants (PTVs) at the CETP gene were associated with plasma lipid levels and CHD.Methods and Results:We sequenced the exons of the CETP gene in 58 469 participants from 12 case-control studies (18 817 CHD cases, 39 652 CHD-free controls). We defined PTV as those that lead to a premature stop, disrupt canonical splice sites, or lead to insertions/deletions that shift frame. We also genotyped 1 Japanese-specific PTV in 27561 participants from 3 case-control studies (14 286 CHD cases, 13 275 CHD-free controls). We tested association of CETP PTV carrier status with both plasma lipids and CHD. Among 58 469 participants with CETP gene-sequencing data available, average age was 51.5 years and 43% were women; 1 in 975 participants carried a PTV at the CETP gene. Compared with noncarriers, carriers of PTV at CETP had higher high-density lipoprotein cholesterol (effect size, 22.6 mg/dL; 95% confidence interval, 18-27; P<1.010-4), lower low-density lipoprotein cholesterol (-12.2 mg/dL; 95% confidence interval, -23 to -0.98; P=0.033), and lower triglycerides (-6.3%; 95% confidence interval, -12 to -0.22; P=0.043). CETP PTV carrier status was associated with reduced risk for CHD (summary odds ratio, 0.70; 95% confidence interval, 0.54-0.90; P=5.110-3).Conclusions:Compared with noncarriers, carriers of PTV at CETP displayed higher high-density lipoprotein cholesterol, lower low-density lipoprotein cholesterol, lower triglycerides, and lower risk for CHD. Rationale:Therapies that inhibit CETP (cholesteryl ester transfer protein) have failed to demonstrate a reduction in risk for coronary heart disease (CHD). Human DNA sequence variants that truncate the CETP gene may provide insight into the efficacy of CETP inhibition.Objective:To test whether protein-truncating variants (PTVs) at the CETP gene were associated with plasma lipid levels and CHD.Methods and Results:We sequenced the exons of the CETP gene in 58 469 participants from 12 case–control studies (18 817 CHD cases, 39 652 CHD-free controls). We defined PTV as those that lead to a premature stop, disrupt canonical splice sites, or lead to insertions/deletions that shift frame. We also genotyped 1 Japanese-specific PTV in 27561 participants from 3 case–control studies (14 286 CHD cases, 13 275 CHD-free controls). We tested association of CETP PTV carrier status with both plasma lipids and CHD. Among 58 469 participants with CETP gene-sequencing data available, average age was 51.5 years and 43% were women; 1 in 975 participants carried a PTV at the CETP gene. Compared with noncarriers, carriers of PTV at CETP had higher high-density lipoprotein cholesterol (effect size, 22.6 mg/dL; 95% confidence interval, 18–27; P<1.0×10−4), lower low-density lipoprotein cholesterol (−12.2 mg/dL; 95% confidence interval, −23 to −0.98; P=0.033), and lower triglycerides (−6.3%; 95% confidence interval, −12 to −0.22; P=0.043). CETP PTV carrier status was associated with reduced risk for CHD (summary odds ratio, 0.70; 95% confidence interval, 0.54–0.90; P=5.1×10−3).Conclusions:Compared with noncarriers, carriers of PTV at CETP displayed higher high-density lipoprotein cholesterol, lower low-density lipoprotein cholesterol, lower triglycerides, and lower risk for CHD. |
| Author | Wang, Jun-Sing Inazu, Akihiro Yamamoto, Ken Watkins, Hugh Zekavat, Seyedeh M. Lavage, Daniel R. Lin, Shih-Yi Elosua, Roberto Teslovich, Tanya M. Leader, Joseph B. Hsiung, Chao A. Kubo, Michiaki Farrall, Martin Hartze, Dustin N. Kato, Norihiro McPherson, Ruth Kawashiri, Masa-aki Ida Chen, Yii-Der Emdin, Connor A. Nakashima, Eitaro Nomura, Akihiro Schunkert, Heribert Lander, Eric S. Saleheen, Danish Asselta, Rosanna Takeuchi, Fumihiko Rader, Daniel J. Tada, Hayato Kirchner, H. Lester Juang, Jyh-Ming J. Kathiresan, Sekar Peloso, Gina M. Marrugat, Jaume Won, Hong-Hee Borecki, Ingrid B. Momozawa, Yukihide McCarthy, Shane Braund, Peter S. Kessler, Thorsten Wilson, James G. Hall, Alistair S. Samani, Nilesh J. Carey, David J. Yamagishi, Masakazu Yokota, Mitsuhiro Khera, Amit V. Merlini, Piera A. Natarajan, Pradeep Ardissino, Diego Willer, Cristen J. Abecasis, Goncalo R. Correa, Adolfo Ito, Kaoru Danesh, John Murray, Michael F. Dewey, Frederick E. Katsuya, Tomohiro Gabriel, Stacey Rotter, Jerome I. Nakatochi, Masahiro Gupta, Namrata Klarin, Derek Duga, St |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28506971$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 2017 American Heart Association, Inc. Copyright Lippincott Williams & Wilkins Ovid Technologies Jun 23, 2017 |
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| Keywords | coronary disease lipids cholesteryl ester transfer protein case-control studies |
| Language | English |
| License | 2017 American Heart Association, Inc. |
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| PublicationTitle | Circulation research |
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| Snippet | Therapies that inhibit CETP (cholesteryl ester transfer protein) have failed to demonstrate a reduction in risk for coronary heart disease (CHD). Human DNA... Rationale:Therapies that inhibit CETP (cholesteryl ester transfer protein) have failed to demonstrate a reduction in risk for coronary heart disease (CHD).... |
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| SubjectTerms | Adult Aged Cardiovascular disease Case-Control Studies CETP gene Cholesterol Cholesterol Ester Transfer Proteins - blood Cholesterol Ester Transfer Proteins - genetics Cholesteryl ester transfer protein Confidence intervals Coronary artery disease Coronary Disease - blood Coronary Disease - diagnosis Coronary Disease - genetics Exons Female Genetic Variation - genetics Health risk assessment Heart diseases Humans Lipids Low density lipoprotein Male Middle Aged Nucleotide sequence Proteins Risk Factors Triglycerides |
| Title | Protein-Truncating Variants at the Cholesteryl Ester Transfer Protein Gene and Risk for Coronary Heart Disease |
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