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

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 ca...
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Autor*in:	Ariel Brautbar [verfasserIn] Salim S. Virani [verfasserIn] John Belmont [verfasserIn] Vijay Nambi [verfasserIn] Peter H. Jones [verfasserIn] Christie M. Ballantyne [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2012

Schlagwörter:	apolipoproteins fibrates genetic variants HDL-C pharmacogenetics

Übergeordnetes Werk:	In: Journal of Lipid Research - Elsevier, 2021, 53(2012), 3, Seite 556-560
Übergeordnetes Werk:	volume:53 ; year:2012 ; number:3 ; pages:556-560

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1194/jlr.M020404

Katalog-ID:	DOAJ072589787

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allfieldsSound	10.1194/jlr.M020404 doi (DE-627)DOAJ072589787 (DE-599)DOAJd8062846a6b24fed9b357832397704ee DE-627 ger DE-627 rakwb eng QD415-436 Ariel Brautbar verfasserin aut 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 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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 cardiovascular disease risk and is commonly treated with combined statin and fibrate therapy. We sought to identify single nucleotide polymorphisms (SNPs) associated with apoC-III level response to combination therapy with statins and fenofibric acid (FA) in individuals with mixed dyslipidemia. Participants (n = 1,250) in a multicenter, randomized, double-blind, active-controlled study examining response to FA alone and in combination with statin were genotyped for candidate SNPs. Multivariate linear regression and two-way ANOVA for percent change in apoC-III level were performed. SNPs in the lipoprotein lipase (LPL) gene region, rs1801177 (P = 4.7 × 10−8), rs7016529 (P = 1.2 × 10−6), and rs249 (P = 4.1 × 10−5), were associated with apoC-III response to combination therapy. A haplotype composed of the minor alleles of these SNPs, with 2% population frequency, was associated with an unexpected apoC-III increase in response to statins and FA. This is the first report to show that genetic variation within the LPL gene region can affect the response of apoC-III levels to combined statin and FA therapy. apolipoproteins fibrates genetic variants HDL-C pharmacogenetics Biochemistry Salim S. Virani verfasserin aut John Belmont verfasserin aut Vijay Nambi verfasserin aut Peter H. Jones verfasserin aut Christie M. Ballantyne verfasserin aut In Journal of Lipid Research Elsevier, 2021 53(2012), 3, Seite 556-560 (DE-627)26601593X (DE-600)1466675-3 15397262 nnns volume:53 year:2012 number:3 pages:556-560 https://doi.org/10.1194/jlr.M020404 kostenfrei https://doaj.org/article/d8062846a6b24fed9b357832397704ee kostenfrei http://www.sciencedirect.com/science/article/pii/S0022227520413719 kostenfrei https://doaj.org/toc/0022-2275 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2006 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 53 2012 3 556-560
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source	In Journal of Lipid Research 53(2012), 3, Seite 556-560 volume:53 year:2012 number:3 pages:556-560
sourceStr	In Journal of Lipid Research 53(2012), 3, Seite 556-560 volume:53 year:2012 number:3 pages:556-560
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topic_facet	apolipoproteins fibrates genetic variants HDL-C pharmacogenetics Biochemistry
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authorswithroles_txt_mv	Ariel Brautbar @@aut@@ Salim S. Virani @@aut@@ John Belmont @@aut@@ Vijay Nambi @@aut@@ Peter H. Jones @@aut@@ Christie M. Ballantyne @@aut@@
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callnumber-first	Q - Science
author	Ariel Brautbar
spellingShingle	Ariel Brautbar misc QD415-436 misc apolipoproteins misc fibrates misc genetic variants misc HDL-C misc pharmacogenetics misc Biochemistry 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
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topic_title	QD415-436 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 apolipoproteins fibrates genetic variants HDL-C pharmacogenetics
topic	misc QD415-436 misc apolipoproteins misc fibrates misc genetic variants misc HDL-C misc pharmacogenetics misc Biochemistry
topic_unstemmed	misc QD415-436 misc apolipoproteins misc fibrates misc genetic variants misc HDL-C misc pharmacogenetics misc Biochemistry
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title	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
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title_full	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
author_sort	Ariel Brautbar
journal	Journal of Lipid Research
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author_browse	Ariel Brautbar Salim S. Virani John Belmont Vijay Nambi Peter H. Jones Christie M. Ballantyne
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title_sort	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
callnumber	QD415-436
title_auth	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
abstract	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 cardiovascular disease risk and is commonly treated with combined statin and fibrate therapy. We sought to identify single nucleotide polymorphisms (SNPs) associated with apoC-III level response to combination therapy with statins and fenofibric acid (FA) in individuals with mixed dyslipidemia. Participants (n = 1,250) in a multicenter, randomized, double-blind, active-controlled study examining response to FA alone and in combination with statin were genotyped for candidate SNPs. Multivariate linear regression and two-way ANOVA for percent change in apoC-III level were performed. SNPs in the lipoprotein lipase (LPL) gene region, rs1801177 (P = 4.7 × 10−8), rs7016529 (P = 1.2 × 10−6), and rs249 (P = 4.1 × 10−5), were associated with apoC-III response to combination therapy. A haplotype composed of the minor alleles of these SNPs, with 2% population frequency, was associated with an unexpected apoC-III increase in response to statins and FA. This is the first report to show that genetic variation within the LPL gene region can affect the response of apoC-III levels to combined statin and FA therapy.
abstractGer	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 cardiovascular disease risk and is commonly treated with combined statin and fibrate therapy. We sought to identify single nucleotide polymorphisms (SNPs) associated with apoC-III level response to combination therapy with statins and fenofibric acid (FA) in individuals with mixed dyslipidemia. Participants (n = 1,250) in a multicenter, randomized, double-blind, active-controlled study examining response to FA alone and in combination with statin were genotyped for candidate SNPs. Multivariate linear regression and two-way ANOVA for percent change in apoC-III level were performed. SNPs in the lipoprotein lipase (LPL) gene region, rs1801177 (P = 4.7 × 10−8), rs7016529 (P = 1.2 × 10−6), and rs249 (P = 4.1 × 10−5), were associated with apoC-III response to combination therapy. A haplotype composed of the minor alleles of these SNPs, with 2% population frequency, was associated with an unexpected apoC-III increase in response to statins and FA. This is the first report to show that genetic variation within the LPL gene region can affect the response of apoC-III levels to combined statin and FA therapy.
abstract_unstemmed	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 cardiovascular disease risk and is commonly treated with combined statin and fibrate therapy. We sought to identify single nucleotide polymorphisms (SNPs) associated with apoC-III level response to combination therapy with statins and fenofibric acid (FA) in individuals with mixed dyslipidemia. Participants (n = 1,250) in a multicenter, randomized, double-blind, active-controlled study examining response to FA alone and in combination with statin were genotyped for candidate SNPs. Multivariate linear regression and two-way ANOVA for percent change in apoC-III level were performed. SNPs in the lipoprotein lipase (LPL) gene region, rs1801177 (P = 4.7 × 10−8), rs7016529 (P = 1.2 × 10−6), and rs249 (P = 4.1 × 10−5), were associated with apoC-III response to combination therapy. A haplotype composed of the minor alleles of these SNPs, with 2% population frequency, was associated with an unexpected apoC-III increase in response to statins and FA. This is the first report to show that genetic variation within the LPL gene region can affect the response of apoC-III levels to combined statin and FA therapy.
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title_short	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
url	https://doi.org/10.1194/jlr.M020404 https://doaj.org/article/d8062846a6b24fed9b357832397704ee http://www.sciencedirect.com/science/article/pii/S0022227520413719 https://doaj.org/toc/0022-2275
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author2	Salim S. Virani John Belmont Vijay Nambi Peter H. Jones Christie M. Ballantyne
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up_date	2024-07-04T01:39:08.617Z
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A haplotype composed of the minor alleles of these SNPs, with 2% population frequency, was associated with an unexpected apoC-III increase in response to statins and FA. This is the first report to show that genetic variation within the LPL gene region can affect the response of apoC-III levels to combined statin and FA therapy.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">apolipoproteins</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">fibrates</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">genetic variants</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">HDL-C</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">pharmacogenetics</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Biochemistry</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Salim S. 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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

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