Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

LPL gene variants affect apoC-III response to combination therapy of statins and fenofibric acid in a randomized clinical trial of individuals with mixed dyslipidemia.

Journal of lipid research - 1 Mar 2012

Brautbar Ariel, Virani Salim S, Belmont John, Nambi Vijay, Jones Peter H, Ballantyne Christie M

Abstract excerpt

ApoC-III is a proatherogenic protein associated with elevated triglycerides; its deficiency is associated with reduced atherosclerosis. Mixed dyslipidemia, characterized by elevated triglyceride and apoC-III levels and low HDL cholesterol level, with or without elevated LDL cholesterol, increases...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Apolipoprotein C-III
Share to Double-Blind Method
Share to Drug Therapy, Combination

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Dyslipidemias

Share to Hydroxymethylglutaryl-CoA Reductase Inhibitors

Share to Lipoprotein Lipase

Share to Regression Analysis

Share to Triglycerides

Source

Open in PubMed Open full text

Identifiers

PMID: 22236405
DOI: 10.1194/jlr.M020404
PMCID: PMC3276479

Genes

LPL

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-22236405-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

LPL gene variants affect apoC-III response to combination therapy of statins and fenofibric acid in a randomized clinical trial of individuals with mixed dyslipidemia.PMID 22236405Read ↗

Rare LPL gene variants attenuate triglyceride reduction and HDL cholesterol increase in response to fenofibric acid therapy in individuals with mixed dyslipidemia.Semantic proximity Read ↗

Interaction between SNPs in the RXRA and near ANGPTL3 gene region inhibits apoB reduction after statin-fenofibric acid therapy in individuals with mixed dyslipidemia.Semantic proximity Read ↗

Variants in the APOA5 gene region and the response to combination therapy with statins and fenofibric acid in a randomized clinical trial of individuals with mixed dyslipidemia.Semantic proximity Read ↗

Genetic variation in the hepatic lipase gene is associated with combined hyperlipidemia, plasma lipid concentrations, and lipid-lowering drug response.Semantic proximity Read ↗

Variants identified in a GWAS meta-analysis for blood lipids are associated with the lipid response to fenofibrate.Semantic proximity Read ↗

Addressing dyslipidemic risk beyond LDL-cholesterol.Semantic proximity Read ↗

Rare APOA5 promoter variants associated with paradoxical HDL cholesterol decrease in response to fenofibric acid therapy.Semantic proximity Read ↗

Gene-diet interactions with polymorphisms of the MGLL gene on plasma low-density lipoprotein cholesterol and size following an omega-3 polyunsaturated fatty acid supplementation: a clinical trial.Semantic proximity Read ↗

Metabolic Characterization of a Rare Genetic Variation Within APOC3 and Its Lipoprotein Lipase-Independent Effects.Semantic proximity Read ↗

Apolipoprotein B genetic variants modify the response to fenofibrate: a GOLDN study.Semantic proximity Read ↗

Additive effects of LPL, APOA5 and APOE variant combinations on triglyceride levels and hypertriglyceridemia: results of the ICARIA genetic sub-study.Semantic proximity Read ↗

Familial combined hypolipidemia: angiopoietin-like protein-3 deficiencySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.