APOA5 gene variants, lipoprotein particle distribution, and progression of coronary heart disease
Animal and human studies support a role for apolipoprotein A-V (apoA-V) in triglyceride (TG) metabolism. We examined the relationship of APOA5 −1131T>C and S19W with lipid subfractions and progression of atherosclerosis in the Lopid Coronary Angiography Trial. Compared with −1131TT men (n = 242),...
| Main Authors: | , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2004-04-01
|
| Series: | Journal of Lipid Research |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0022227520318605 |
| _version_ | 1818715720807088128 |
|---|---|
| author | Philippa J. Talmud Steve Martin Marja-Riitta Taskinen M. Heikki Frick Markku S. Nieminen Y. Antero Kesäniemi Amos Pasternack Steve E. Humphries Mikko Syvänne |
| author_facet | Philippa J. Talmud Steve Martin Marja-Riitta Taskinen M. Heikki Frick Markku S. Nieminen Y. Antero Kesäniemi Amos Pasternack Steve E. Humphries Mikko Syvänne |
| author_sort | Philippa J. Talmud |
| collection | DOAJ |
| description | Animal and human studies support a role for apolipoprotein A-V (apoA-V) in triglyceride (TG) metabolism. We examined the relationship of APOA5 −1131T>C and S19W with lipid subfractions and progression of atherosclerosis in the Lopid Coronary Angiography Trial. Compared with −1131TT men (n = 242), carriers of the −1131C allele (n = 54) had significantly higher total TG (P = 0.03), reflected in significantly increased VLDL mass [higher VLDL-TG, VLDL-cholesterol, VLDL-protein, and surface lipids (all P < 0.05)]. Because apoB levels were unaffected by genotype, this suggests an increase in VLDL size and not number. Compared with 19SS men (n = 268), 19W carriers (n = 44) had higher intermediate density lipoprotein (IDL)-TG, IDL-cholesterol (P = 0.04), and IDL-surface components [free cholesterol (P = 0.005) and phospholipids (P = 0.017)] but not protein content, suggesting an increase in IDL lipid enrichment resulting in an increase in IDL size. 19W carriers also showed a trend toward increased progression of atherogenesis, as measured by change in average diameter of segments (−0.46 ± 0.011 mm compared with −0.016 ± 0.006 mm) in 19SS men (P = 0.08). There was no effect of genotype on the response of these parameters to gemfibrozil treatment.These results shed new light on the role of APOA5 variants in TG metabolism and coronary heart disease risk. |
| first_indexed | 2024-12-17T19:07:51Z |
| format | Article |
| id | doaj.art-e4355aba2fd5494a85eb9709ed8447a2 |
| institution | Directory Open Access Journal |
| issn | 0022-2275 |
| language | English |
| last_indexed | 2024-12-17T19:07:51Z |
| publishDate | 2004-04-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Lipid Research |
| spelling | doaj.art-e4355aba2fd5494a85eb9709ed8447a22022-12-21T21:35:57ZengElsevierJournal of Lipid Research0022-22752004-04-01454750756APOA5 gene variants, lipoprotein particle distribution, and progression of coronary heart diseasePhilippa J. Talmud0Steve Martin1Marja-Riitta Taskinen2M. Heikki Frick3Markku S. Nieminen4Y. Antero Kesäniemi5Amos Pasternack6Steve E. Humphries7Mikko Syvänne8Centre for Cardiovascular Genetics, Department of Medicine, British Heart Foundation Laboratories, Royal Free and University College Medical School, London, UK; Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland; Department of Medicine and Biocenter Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland; Department of Medicine, Tampere University Hospital, Tampere, FinlandCentre for Cardiovascular Genetics, Department of Medicine, British Heart Foundation Laboratories, Royal Free and University College Medical School, London, UK; Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland; Department of Medicine and Biocenter Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland; Department of Medicine, Tampere University Hospital, Tampere, FinlandCentre for Cardiovascular Genetics, Department of Medicine, British Heart Foundation Laboratories, Royal Free and University College Medical School, London, UK; Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland; Department of Medicine and Biocenter Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland; Department of Medicine, Tampere University Hospital, Tampere, FinlandCentre for Cardiovascular Genetics, Department of Medicine, British Heart Foundation Laboratories, Royal Free and University College Medical School, London, UK; Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland; Department of Medicine and Biocenter Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland; Department of Medicine, Tampere University Hospital, Tampere, FinlandCentre for Cardiovascular Genetics, Department of Medicine, British Heart Foundation Laboratories, Royal Free and University College Medical School, London, UK; Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland; Department of Medicine and Biocenter Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland; Department of Medicine, Tampere University Hospital, Tampere, FinlandCentre for Cardiovascular Genetics, Department of Medicine, British Heart Foundation Laboratories, Royal Free and University College Medical School, London, UK; Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland; Department of Medicine and Biocenter Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland; Department of Medicine, Tampere University Hospital, Tampere, FinlandCentre for Cardiovascular Genetics, Department of Medicine, British Heart Foundation Laboratories, Royal Free and University College Medical School, London, UK; Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland; Department of Medicine and Biocenter Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland; Department of Medicine, Tampere University Hospital, Tampere, FinlandCentre for Cardiovascular Genetics, Department of Medicine, British Heart Foundation Laboratories, Royal Free and University College Medical School, London, UK; Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland; Department of Medicine and Biocenter Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland; Department of Medicine, Tampere University Hospital, Tampere, FinlandCentre for Cardiovascular Genetics, Department of Medicine, British Heart Foundation Laboratories, Royal Free and University College Medical School, London, UK; Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland; Department of Medicine and Biocenter Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland; Department of Medicine, Tampere University Hospital, Tampere, FinlandAnimal and human studies support a role for apolipoprotein A-V (apoA-V) in triglyceride (TG) metabolism. We examined the relationship of APOA5 −1131T>C and S19W with lipid subfractions and progression of atherosclerosis in the Lopid Coronary Angiography Trial. Compared with −1131TT men (n = 242), carriers of the −1131C allele (n = 54) had significantly higher total TG (P = 0.03), reflected in significantly increased VLDL mass [higher VLDL-TG, VLDL-cholesterol, VLDL-protein, and surface lipids (all P < 0.05)]. Because apoB levels were unaffected by genotype, this suggests an increase in VLDL size and not number. Compared with 19SS men (n = 268), 19W carriers (n = 44) had higher intermediate density lipoprotein (IDL)-TG, IDL-cholesterol (P = 0.04), and IDL-surface components [free cholesterol (P = 0.005) and phospholipids (P = 0.017)] but not protein content, suggesting an increase in IDL lipid enrichment resulting in an increase in IDL size. 19W carriers also showed a trend toward increased progression of atherogenesis, as measured by change in average diameter of segments (−0.46 ± 0.011 mm compared with −0.016 ± 0.006 mm) in 19SS men (P = 0.08). There was no effect of genotype on the response of these parameters to gemfibrozil treatment.These results shed new light on the role of APOA5 variants in TG metabolism and coronary heart disease risk.http://www.sciencedirect.com/science/article/pii/S0022227520318605apolipoprotein A-Vlipid subfractionsvery low density lipoproteinintermediate density lipoproteinprogression of atherogenesisLopid Coronary Angiography Trial |
| spellingShingle | Philippa J. Talmud Steve Martin Marja-Riitta Taskinen M. Heikki Frick Markku S. Nieminen Y. Antero Kesäniemi Amos Pasternack Steve E. Humphries Mikko Syvänne APOA5 gene variants, lipoprotein particle distribution, and progression of coronary heart disease Journal of Lipid Research apolipoprotein A-V lipid subfractions very low density lipoprotein intermediate density lipoprotein progression of atherogenesis Lopid Coronary Angiography Trial |
| title | APOA5 gene variants, lipoprotein particle distribution, and progression of coronary heart disease |
| title_full | APOA5 gene variants, lipoprotein particle distribution, and progression of coronary heart disease |
| title_fullStr | APOA5 gene variants, lipoprotein particle distribution, and progression of coronary heart disease |
| title_full_unstemmed | APOA5 gene variants, lipoprotein particle distribution, and progression of coronary heart disease |
| title_short | APOA5 gene variants, lipoprotein particle distribution, and progression of coronary heart disease |
| title_sort | apoa5 gene variants lipoprotein particle distribution and progression of coronary heart disease |
| topic | apolipoprotein A-V lipid subfractions very low density lipoprotein intermediate density lipoprotein progression of atherogenesis Lopid Coronary Angiography Trial |
| url | http://www.sciencedirect.com/science/article/pii/S0022227520318605 |
| work_keys_str_mv | AT philippajtalmud apoa5genevariantslipoproteinparticledistributionandprogressionofcoronaryheartdisease AT stevemartin apoa5genevariantslipoproteinparticledistributionandprogressionofcoronaryheartdisease AT marjariittataskinen apoa5genevariantslipoproteinparticledistributionandprogressionofcoronaryheartdisease AT mheikkifrick apoa5genevariantslipoproteinparticledistributionandprogressionofcoronaryheartdisease AT markkusnieminen apoa5genevariantslipoproteinparticledistributionandprogressionofcoronaryheartdisease AT yanterokesaniemi apoa5genevariantslipoproteinparticledistributionandprogressionofcoronaryheartdisease AT amospasternack apoa5genevariantslipoproteinparticledistributionandprogressionofcoronaryheartdisease AT steveehumphries apoa5genevariantslipoproteinparticledistributionandprogressionofcoronaryheartdisease AT mikkosyvanne apoa5genevariantslipoproteinparticledistributionandprogressionofcoronaryheartdisease |