ArticleAtherosclerosis2011
Association of gene variants with lipid levels in response to fenofibrate is influenced by metabolic syndrome status.
Article in Atherosclerosis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- One Diet Does Not Fit All: A Systematic Review and Meta-Analysis of Gene-Diet Interactions Affecting Blood Lipid Profiles.Current issues in molecular biology · 2026Review
- Fibrate pharmacogenomics: expanding past the genome.Pharmacogenomics · 2020Article
- An epigenome-wide association study of inflammatory response to fenofibrate in the Genetics of Lipid Lowering Drugs and Diet Network.Pharmacogenomics · 2017Article
- DNA methylation as a marker of response in rheumatoid arthritis.Pharmacogenomics · 2017Review
- Functional variants of lipid level modifier MLXIPL, GCKR, GALNT2, CILP2, ANGPTL3 and TRIB1 genes in healthy Roma and Hungarian populations.Pathology oncology research : POR · 2015Article
- Lipid changes due to fenofibrate treatment are not associated with changes in DNA methylation patterns in the GOLDN study.Frontiers in genetics · 2015Article
- Gene polymorphisms and gene scores linked to low serum carotenoid status and their associations with metabolic disturbance and depressive symptoms in African-American adults.The British journal of nutrition · 2014Article
- Central obesity in males affected by a dyslipidemia-associated genetic polymorphism on APOA1/C3/A4/A5 gene cluster.Nutrition & diabetes · 2013Article
- Pharmacogenomics of high-density lipoprotein-cholesterol-raising therapies.Expert review of cardiovascular therapy · 2013Review
- The paradox of ApoA5 modulation of triglycerides: evidence from clinical and basic research.Clinical biochemistry · 2013Review
- Triglyceride level-influencing functional variants of the ANGPTL3, CILP2, and TRIB1 loci in ischemic stroke.Neuromolecular medicine · 2011Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
objectiveFenofibrate therapy reduces serum triglycerides (TG) and increases high-density lipoprotein-cholesterol (HDL-C) and thus addresses the atherogenic dyslipidemia associated with metabolic syndrome (MetS). Our hypothesis is that genetic factors contribute to the variability of lipid response to fenofibrate differently in subjects with MetS and without MetS.
methodsWe investigated the association in 25 candidate genes with lipid responses to a 3-weeks trial on fenofibrate in subjects with and without MetS. We employed growth curve mixed models to generate the response phenotypes to fenofibrate in TG, HDL-C, and low-density lipoprotein-cholesterol (LDL-C) and examined the genetic associations accounting for family dependencies.
resultsAfter correcting for multiple testing (p<0.05) and accounting for significant differences in the association effect sizes between subjects with and without MetS (p<0.05), variants of APOA5 (rs662799) and APOE (rs429358) were associated with HDL-C and LDL-C responses in MetS subjects, while APOA4 (rs675) was associated with TG response in non-MetS subjects. There was also suggestive evidence that MetS may interact with APOA4 (p=0.017), APOA5 (p=0.06), and APOE (p=0.09) to the variation to lipid responses.
conclusionsGenetic effects that contributed to the variability of lipid responses to fenofibrate may differ in subjects with and without MetS. This research may provide guidance for more personalized and effective therapies.
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