Common APOC3 variants are associated with circulating ApoC-III and VLDL cholesterol but not with total apolipoprotein B and coronary artery disease.


Journal

Atherosclerosis
ISSN: 1879-1484
Titre abrégé: Atherosclerosis
Pays: Ireland
ID NLM: 0242543

Informations de publication

Date de publication:
10 2020
Historique:
received: 30 03 2020
revised: 28 07 2020
accepted: 25 08 2020
pubmed: 20 9 2020
medline: 24 6 2021
entrez: 19 9 2020
Statut: ppublish

Résumé

Very rare loss-of-function mutations in the apolipoprotein C3 (APOC3) gene have been associated with low circulating apoC-III, low triglycerides, and reduced cardiovascular risk. We aimed to analyze the impact of common APOC3 variants on key parameters of lipid metabolism and coronary artery disease in the largest sample so far. Common variants in APOC3 were tested for associations with circulating apoC-III, lipids, and apolipoprotein B (apoB) in 3041 participants of the LUdwigshafen RIsk and Cardiovascular health study (LURIC). These variants were then tested for associations with coronary artery disease in a meta-analysis comprising up to 332,389 participants of the CARDIOGRAMplusC4D consortium and the UK Biobank. The mean (standard deviation) apoC-III concentration was 14.6 (5.1) mg/dl. Seven common variants in APOC3 (rs734104, rs4520, rs5142, rs5141, rs5130, rs5128, and rs4225) were associated with circulating apoC-III (all p < 0.05). The alleles that modestly raised apoC-III were also associated with markedly higher total triglycerides and very low density lipoprotein (VLDL) triglycerides and cholesterol (all p < 0.05), but not with low density lipoprotein (LDL) cholesterol and total apoB (all p > 0.05). These variants were not associated with coronary artery disease in the CARDIOGRAMplusC4D consortium and the UK Biobank (all p > 0.1). Modest, genetically caused elevations of apoC-III are associated with a marked increase of triglyceride-rich lipoproteins but not with an increase of LDL cholesterol, total apoB, and coronary artery disease. Whether effective inhibition of apoC-III production with antisense oligomers will be instrumental to reduce cardiovascular risk remains to be demonstrated.

Sections du résumé

BACKGROUND AND AIMS
Very rare loss-of-function mutations in the apolipoprotein C3 (APOC3) gene have been associated with low circulating apoC-III, low triglycerides, and reduced cardiovascular risk. We aimed to analyze the impact of common APOC3 variants on key parameters of lipid metabolism and coronary artery disease in the largest sample so far.
METHODS
Common variants in APOC3 were tested for associations with circulating apoC-III, lipids, and apolipoprotein B (apoB) in 3041 participants of the LUdwigshafen RIsk and Cardiovascular health study (LURIC). These variants were then tested for associations with coronary artery disease in a meta-analysis comprising up to 332,389 participants of the CARDIOGRAMplusC4D consortium and the UK Biobank.
RESULTS
The mean (standard deviation) apoC-III concentration was 14.6 (5.1) mg/dl. Seven common variants in APOC3 (rs734104, rs4520, rs5142, rs5141, rs5130, rs5128, and rs4225) were associated with circulating apoC-III (all p < 0.05). The alleles that modestly raised apoC-III were also associated with markedly higher total triglycerides and very low density lipoprotein (VLDL) triglycerides and cholesterol (all p < 0.05), but not with low density lipoprotein (LDL) cholesterol and total apoB (all p > 0.05). These variants were not associated with coronary artery disease in the CARDIOGRAMplusC4D consortium and the UK Biobank (all p > 0.1).
CONCLUSIONS
Modest, genetically caused elevations of apoC-III are associated with a marked increase of triglyceride-rich lipoproteins but not with an increase of LDL cholesterol, total apoB, and coronary artery disease. Whether effective inhibition of apoC-III production with antisense oligomers will be instrumental to reduce cardiovascular risk remains to be demonstrated.

Identifiants

pubmed: 32949947
pii: S0021-9150(20)30461-5
doi: 10.1016/j.atherosclerosis.2020.08.017
pii:
doi:

Substances chimiques

Apolipoprotein C-III 0
Apolipoproteins B 0
Cholesterol, VLDL 0
Lipoproteins, VLDL 0
Triglycerides 0

Types de publication

Journal Article Meta-Analysis Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

84-90

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Auteurs

Günther Silbernagel (G)

Division of Angiology, Department of Internal Medicine, Medical University of Graz, Austria; Department of Cardiology, Charité-Universitätsmedizin Berlin (CBF), Berlin Institute of Health (BIH), DZHK (German Center for Cardiovascular Research) e.V., Partner Site Berlin, Berlin, Germany.

Hubert Scharnagl (H)

Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Graz, Austria. Electronic address: hubert.scharnagl@medunigraz.at.

Marcus E Kleber (ME)

Department of Internal Medicine 5 (Nephrology, Hypertensiology, Endocrinology, Diabetology, Rheumatology), Mannheim Medical Faculty, University of Heidelberg, Mannheim, Germany.

Michael M Hoffmann (MM)

Institute of Clinical Chemistry and Laboratory Medicine, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Graciela Delgado (G)

Department of Internal Medicine 5 (Nephrology, Hypertensiology, Endocrinology, Diabetology, Rheumatology), Mannheim Medical Faculty, University of Heidelberg, Mannheim, Germany.

Tatjana Stojakovic (T)

Clinical Institute of Medical and Chemical Laboratory Diagnostics, University Hospital Graz, Graz, Austria.

Thomas Gary (T)

Division of Angiology, Department of Internal Medicine, Medical University of Graz, Austria.

Lingyao Zeng (L)

Deutsches Herzzentrum München, Klinik für Herz- und Kreislauferkrankungen, Technische Universität München, DZHK (German Center for Cardiovascular Research) e.V., Partner Site Munich Heart Alliance, Munich, Germany.

Andreas Ritsch (A)

Department of Internal Medicine, Medical University of Innsbruck, Innsbruck, Austria.

Stephen Zewinger (S)

Department of Internal Medicine 4 (Nephrology and Hypertension), University of Homburg, Homburg/Saar, Germany.

Thimoteus Speer (T)

Department of Internal Medicine 4 (Nephrology and Hypertension), University of Homburg, Homburg/Saar, Germany.

Heribert Schunkert (H)

Deutsches Herzzentrum München, Klinik für Herz- und Kreislauferkrankungen, Technische Universität München, DZHK (German Center for Cardiovascular Research) e.V., Partner Site Munich Heart Alliance, Munich, Germany.

Ulf Landmesser (U)

Department of Cardiology, Charité-Universitätsmedizin Berlin (CBF), Berlin Institute of Health (BIH), DZHK (German Center for Cardiovascular Research) e.V., Partner Site Berlin, Berlin, Germany.

Winfried März (W)

Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Graz, Austria; Department of Internal Medicine 5 (Nephrology, Hypertensiology, Endocrinology, Diabetology, Rheumatology), Mannheim Medical Faculty, University of Heidelberg, Mannheim, Germany; Synlab Academy, Synlab Holding Germany GmbH, Mannheim, Germany.

Tanja B Grammer (TB)

Mannheimer Institute for Public Health, Mannheim Medical Faculty, University of Heidelberg, Mannheim, Germany.

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Classifications MeSH