Excess of rare variants in genes identified by genome-wide association study of hypertriglyceridemia
Open accessAbstract
Genome-wide association studies (GWAS) have identified multiple loci associated with plasma lipid concentrations. Common variants at these loci together explain <10% of variation in each lipid trait. Rare variants with large individual effects may also contribute to the heritability of lipid traits; however, the extent to which rare variants affect lipid phenotypes remains to be determined. Here we show an accumulation of rare variants, or a mutation skew, in GWAS-identified genes in individuals with hypertriglyceridemia (HTG). Through GWAS, we identified common variants in APOA5, GCKR, LPL and APOB associated with HTG. Resequencing of these genes revealed a significant burden of 154 rare missense or nonsense variants in 438 individuals with HTG, compared to 53 variants in 327 controls (P = 6.2 x 10(-8)), corresponding to a carrier frequency of 28.1% of affected individuals and 15.3% of controls (P = 2.6 x 10(-5)). Considering rare variants in these genes incrementally increased the proportion of genetic variation contributing to HTG.
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Four hypertriglyceridemia genes showed a significant excess of rare coding variants.
“whereas a significant excess of rare coding variants was found in 4 genes for hypertriglyceridemia116.”
From Rare and common variants: twenty arguments (2012) · cites this paper as [116]
Common variants in APOA5, GCKR, LPL, and APOB have been identified, supporting a role for both common and rare variants responsible for hypertriglyceridemia.
“Specifically, common variants in APOA5, glucose kinase regulatory protein (GCKR), LPL, and APOB have been identified, thereby supporting a role for both common and rare variants responsible for hypertriglyceridemia. 151”
From Triglycerides and Cardiovascular Disease: A Scientific Statement From the American Heart Association (2011) · cites this paper as [151]
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- Authors
- Johansen, C. T., Wang, J., Lanktree, M. B., Cao, H., McIntyre, A. D., Ban, M. R., Martins, R. A., Kennedy, B. A., Hassell, R. G., Visser, M. E., Schwartz, S. M., Voight, B. F., Elosua, R., Salomaa, V., O'Donnell, C. J., Dallinga-Thie, G. M., Anand, S. S., Yusuf, S., Huff, M. W., Kathiresan, S., & Hegele, R. A.
- Affiliations
- Western University (CA)
- Amsterdam UMC Location University of Amsterdam (NL)
- University of Washington (US)
- Broad Institute (US)
- Finnish Institute for Health and Welfare (FI)
- Population Health Research Institute (CA)
- Corresponding author
- Hegele, Robert A
- ORCID
- Venue
- Nature Genetics
- Published
- 2010-07-25
- Volume
- 42
- Issue
- 8
- Pages
- 684-687
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC3017369
- OpenAlex
- W2149813409
- Cited by
- 437
- References
- 26
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 3 · 2023: 8 · 2022: 8 · 2021: 8 · 2020: 15 · 2019: 17 · 2018: 16 · 2017: 21 · 2016: 26 · 2015: 37 · 2014: 52 · 2013: 52 · 2012: 62
- FWCI
- 46.76
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Scholarship@Western (Western University) (submittedVersion)
- STM:n Hallinnonalan avoin julkaisuarkisto (Julkari) (submittedVersion)
- Funders
- National Institutes of Health (6u54rr020278-06)
- Canadian Institutes of Health Research (79853_1, 79523_1, MOP13430)
- National Heart, Lung, and Blood Institute (R01HL087676)
- National Center for Research Resources (U54-RR020278)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Keywords
- hypertriglyceridemia, rare variants, mutational burden, APOA5, GCKR, lipoprotein lipase, apolipoprotein B, heritability, candidate genes
- MeSH terms
- Apolipoprotein A-V, Adult, Apolipoproteins A, Female, Genes, Genetic Testing, Humans, Lipids, Lipoprotein Lipase, Male, Middle Aged, Phenotype, Genetic Variation, Hypertriglyceridemia, Cohort Studies, Adaptor Proteins, Signal Transducing, Genome-Wide Association Study
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