ApoC-III gene polymorphisms and risk of coronary artery disease
Several polymorphisms in the apolipoprotein C-III (apoC-III) gene have been associated with hypertriglyceridemia, but the link with coronary artery disease risk is still controversial. In particular, apoC-III promoter sequence variants in the insulin responsive element (IRE), constitutively resistan...
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| Format: | Article |
| Language: | English |
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Elsevier
2002-09-01
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| Series: | Journal of Lipid Research |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S002222752032808X |
| _version_ | 1830190466443771904 |
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| author | Oliviero Olivieri Chiara Stranieri Antonella Bassi Barbara Zaia Domenico Girelli Francesca Pizzolo Elisabetta Trabetti Suzanne Cheng Michael A. Grow Pier Franco Pignatti Roberto Corrocher |
| author_facet | Oliviero Olivieri Chiara Stranieri Antonella Bassi Barbara Zaia Domenico Girelli Francesca Pizzolo Elisabetta Trabetti Suzanne Cheng Michael A. Grow Pier Franco Pignatti Roberto Corrocher |
| author_sort | Oliviero Olivieri |
| collection | DOAJ |
| description | Several polymorphisms in the apolipoprotein C-III (apoC-III) gene have been associated with hypertriglyceridemia, but the link with coronary artery disease risk is still controversial. In particular, apoC-III promoter sequence variants in the insulin responsive element (IRE), constitutively resistant to downregulation by insulin, have never been investigated in this connection. We studied a total of 800 patients, 549 of whom had angiographically documented coronary atherosclerosis, whereas 251 had normal coronary arteriograms. We measured plasma lipids, insulin, apoA-I, apoB, and apoC-III and assessed three polymorphisms in the apoC-III gene, namely, T-455C in the IRE promoter region, C1100T in exon 3, and Sst1 polymorphic site (S1/S2) in the 3′ untranslated region. Each variant influenced triglyceride levels, but only the T-455C (in homozygosity) and S2 alleles influenced apoC-III levels. In coronary artery disease (CAD) patients, 18.6% were homozygous for the −455C variant compared with only 9.2% in CAD-free group (P < 0.001).In logistic regression models, homozygosity for −455C variant was associated with a significantly increased risk of CAD (OR = 2.5 and 2.18 for unadjusted and adjusted models, respectively) suggesting that it represents an independent genetic susceptibility factor for CAD. |
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| institution | Directory Open Access Journal |
| issn | 0022-2275 |
| language | English |
| last_indexed | 2024-12-17T23:22:24Z |
| publishDate | 2002-09-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Lipid Research |
| spelling | doaj.art-6522f154239d40aa84e57a6f535bb57e2022-12-21T21:28:51ZengElsevierJournal of Lipid Research0022-22752002-09-0143914501457ApoC-III gene polymorphisms and risk of coronary artery diseaseOliviero Olivieri0Chiara Stranieri1Antonella Bassi2Barbara Zaia3Domenico Girelli4Francesca Pizzolo5Elisabetta Trabetti6Suzanne Cheng7Michael A. Grow8Pier Franco Pignatti9Roberto Corrocher10Unit of Internal Medicine, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Clinical and Experimental Medicine, Section of Biology and Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Mother and Child, and Biology-Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Human Genetics, Roche Molecular System, Alameda, CA, USAUnit of Internal Medicine, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Clinical and Experimental Medicine, Section of Biology and Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Mother and Child, and Biology-Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Human Genetics, Roche Molecular System, Alameda, CA, USAUnit of Internal Medicine, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Clinical and Experimental Medicine, Section of Biology and Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Mother and Child, and Biology-Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Human Genetics, Roche Molecular System, Alameda, CA, USAUnit of Internal Medicine, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Clinical and Experimental Medicine, Section of Biology and Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Mother and Child, and Biology-Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Human Genetics, Roche Molecular System, Alameda, CA, USAUnit of Internal Medicine, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Clinical and Experimental Medicine, Section of Biology and Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Mother and Child, and Biology-Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Human Genetics, Roche Molecular System, Alameda, CA, USAUnit of Internal Medicine, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Clinical and Experimental Medicine, Section of Biology and Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Mother and Child, and Biology-Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Human Genetics, Roche Molecular System, Alameda, CA, USAUnit of Internal Medicine, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Clinical and Experimental Medicine, Section of Biology and Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Mother and Child, and Biology-Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Human Genetics, Roche Molecular System, Alameda, CA, USAUnit of Internal Medicine, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Clinical and Experimental Medicine, Section of Biology and Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Mother and Child, and Biology-Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Human Genetics, Roche Molecular System, Alameda, CA, USAUnit of Internal Medicine, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Clinical and Experimental Medicine, Section of Biology and Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Mother and Child, and Biology-Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Human Genetics, Roche Molecular System, Alameda, CA, USAUnit of Internal Medicine, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Clinical and Experimental Medicine, Section of Biology and Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Mother and Child, and Biology-Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Human Genetics, Roche Molecular System, Alameda, CA, USAUnit of Internal Medicine, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Clinical and Experimental Medicine, Section of Biology and Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Mother and Child, and Biology-Genetics, Institute of Clinical Chemistry, University of Verona, Verona, Italy; Department of Human Genetics, Roche Molecular System, Alameda, CA, USASeveral polymorphisms in the apolipoprotein C-III (apoC-III) gene have been associated with hypertriglyceridemia, but the link with coronary artery disease risk is still controversial. In particular, apoC-III promoter sequence variants in the insulin responsive element (IRE), constitutively resistant to downregulation by insulin, have never been investigated in this connection. We studied a total of 800 patients, 549 of whom had angiographically documented coronary atherosclerosis, whereas 251 had normal coronary arteriograms. We measured plasma lipids, insulin, apoA-I, apoB, and apoC-III and assessed three polymorphisms in the apoC-III gene, namely, T-455C in the IRE promoter region, C1100T in exon 3, and Sst1 polymorphic site (S1/S2) in the 3′ untranslated region. Each variant influenced triglyceride levels, but only the T-455C (in homozygosity) and S2 alleles influenced apoC-III levels. In coronary artery disease (CAD) patients, 18.6% were homozygous for the −455C variant compared with only 9.2% in CAD-free group (P < 0.001).In logistic regression models, homozygosity for −455C variant was associated with a significantly increased risk of CAD (OR = 2.5 and 2.18 for unadjusted and adjusted models, respectively) suggesting that it represents an independent genetic susceptibility factor for CAD.http://www.sciencedirect.com/science/article/pii/S002222752032808Xlipidsrisk factorsinsulin |
| spellingShingle | Oliviero Olivieri Chiara Stranieri Antonella Bassi Barbara Zaia Domenico Girelli Francesca Pizzolo Elisabetta Trabetti Suzanne Cheng Michael A. Grow Pier Franco Pignatti Roberto Corrocher ApoC-III gene polymorphisms and risk of coronary artery disease Journal of Lipid Research lipids risk factors insulin |
| title | ApoC-III gene polymorphisms and risk of coronary artery disease |
| title_full | ApoC-III gene polymorphisms and risk of coronary artery disease |
| title_fullStr | ApoC-III gene polymorphisms and risk of coronary artery disease |
| title_full_unstemmed | ApoC-III gene polymorphisms and risk of coronary artery disease |
| title_short | ApoC-III gene polymorphisms and risk of coronary artery disease |
| title_sort | apoc iii gene polymorphisms and risk of coronary artery disease |
| topic | lipids risk factors insulin |
| url | http://www.sciencedirect.com/science/article/pii/S002222752032808X |
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