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APOE genotype influences insulin resistance, apolipoprotein CII and CIII according to plasma fatty acid profile in the Metabolic Syndrome
Metabolic markers associated with the Metabolic Syndrome (MetS) may be affected by interactions between the APOE genotype and plasma fatty acids (FA). In this study, we explored FA-gene interactions between the missense APOE polymorphisms and FA status on metabolic markers in MetS. Plasma FA, blood...
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Published in: | Scientific reports 2017-07, Vol.7 (1), p.6274-10, Article 6274 |
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creator | Fallaize, Rosalind Carvalho-Wells, Andrew L. Tierney, Audrey C. Marin, Carmen Kieć-Wilk, Beata Dembińska-Kieć, Aldona Drevon, Christian A. DeFoort, Catherine Lopez-Miranda, José Risérus, Ulf Saris, Wim H. Blaak, Ellen E. Roche, Helen M. Lovegrove, Julie A. |
description | Metabolic markers associated with the Metabolic Syndrome (MetS) may be affected by interactions between the
APOE
genotype and plasma fatty acids (FA). In this study, we explored FA-gene interactions between the missense
APOE
polymorphisms and FA status on metabolic markers in MetS. Plasma FA, blood pressure, insulin sensitivity and lipid concentrations were determined at baseline and following a 12-week randomized, controlled, parallel, dietary FA intervention in 442 adults with MetS (LIPGENE study). FA-
APOE
gene interactions at baseline and following change in plasma FA were assessed using adjusted general linear models. At baseline
E4
carriers had higher plasma concentrations of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apo B) compared with
E2
carriers; and higher TC, LDL-C and apo B compared with
E3/E3
. Whilst elevated plasma n-3 polyunsaturated FA (PUFA) was associated with a beneficially lower concentration of apo CIII in
E2
carriers, a high proportion of plasma C16:0 was associated with insulin resistance in
E4
carriers. Following FA intervention, a reduction in plasma long-chain n-3 PUFA was associated with a reduction in apo CII concentration in
E2
carriers. Our novel data suggest that individuals with MetS may benefit from personalized dietary interventions based on
APOE
genotype. |
doi_str_mv | 10.1038/s41598-017-05802-2 |
format | article |
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APOE
genotype and plasma fatty acids (FA). In this study, we explored FA-gene interactions between the missense
APOE
polymorphisms and FA status on metabolic markers in MetS. Plasma FA, blood pressure, insulin sensitivity and lipid concentrations were determined at baseline and following a 12-week randomized, controlled, parallel, dietary FA intervention in 442 adults with MetS (LIPGENE study). FA-
APOE
gene interactions at baseline and following change in plasma FA were assessed using adjusted general linear models. At baseline
E4
carriers had higher plasma concentrations of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apo B) compared with
E2
carriers; and higher TC, LDL-C and apo B compared with
E3/E3
. Whilst elevated plasma n-3 polyunsaturated FA (PUFA) was associated with a beneficially lower concentration of apo CIII in
E2
carriers, a high proportion of plasma C16:0 was associated with insulin resistance in
E4
carriers. Following FA intervention, a reduction in plasma long-chain n-3 PUFA was associated with a reduction in apo CII concentration in
E2
carriers. Our novel data suggest that individuals with MetS may benefit from personalized dietary interventions based on
APOE
genotype.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-017-05802-2</identifier><identifier>PMID: 28740125</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>45/22 ; 45/23 ; 631/208/212/2130 ; 692/163/2743/2037 ; 692/53/2421 ; 692/700/459/284 ; 82/16 ; Adult ; Aged ; Apolipoprotein B ; Apolipoprotein C-II - metabolism ; Apolipoprotein C-III ; Apolipoprotein CII ; Apolipoprotein E ; Apolipoprotein E4 ; Apolipoproteins ; Apolipoproteins E - genetics ; Blood pressure ; Cholesterol ; Diet ; Fatty acids ; Fatty Acids - blood ; Female ; Genotype ; Genotype & phenotype ; Humanities and Social Sciences ; Humans ; Insulin ; Insulin Resistance ; Lipids - analysis ; Low density lipoprotein ; Male ; Metabolic disorders ; Metabolic syndrome ; Metabolic Syndrome - blood ; Metabolic Syndrome - genetics ; Metabolic Syndrome - pathology ; Middle Aged ; multidisciplinary ; Polymorphism, Genetic ; Polyunsaturated fatty acids ; Science ; Science (multidisciplinary)</subject><ispartof>Scientific reports, 2017-07, Vol.7 (1), p.6274-10, Article 6274</ispartof><rights>The Author(s) 2017</rights><rights>2017. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c577t-6f5ac17190977ee301c1ef850ea4ae14cc6b2249c614bc96c61d772bc4291be83</citedby><cites>FETCH-LOGICAL-c577t-6f5ac17190977ee301c1ef850ea4ae14cc6b2249c614bc96c61d772bc4291be83</cites><orcidid>0000-0003-3734-6489</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1956172897/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1956172897?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28740125$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-333525$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Fallaize, Rosalind</creatorcontrib><creatorcontrib>Carvalho-Wells, Andrew L.</creatorcontrib><creatorcontrib>Tierney, Audrey C.</creatorcontrib><creatorcontrib>Marin, Carmen</creatorcontrib><creatorcontrib>Kieć-Wilk, Beata</creatorcontrib><creatorcontrib>Dembińska-Kieć, Aldona</creatorcontrib><creatorcontrib>Drevon, Christian A.</creatorcontrib><creatorcontrib>DeFoort, Catherine</creatorcontrib><creatorcontrib>Lopez-Miranda, José</creatorcontrib><creatorcontrib>Risérus, Ulf</creatorcontrib><creatorcontrib>Saris, Wim H.</creatorcontrib><creatorcontrib>Blaak, Ellen E.</creatorcontrib><creatorcontrib>Roche, Helen M.</creatorcontrib><creatorcontrib>Lovegrove, Julie A.</creatorcontrib><title>APOE genotype influences insulin resistance, apolipoprotein CII and CIII according to plasma fatty acid profile in the Metabolic Syndrome</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Metabolic markers associated with the Metabolic Syndrome (MetS) may be affected by interactions between the
APOE
genotype and plasma fatty acids (FA). In this study, we explored FA-gene interactions between the missense
APOE
polymorphisms and FA status on metabolic markers in MetS. Plasma FA, blood pressure, insulin sensitivity and lipid concentrations were determined at baseline and following a 12-week randomized, controlled, parallel, dietary FA intervention in 442 adults with MetS (LIPGENE study). FA-
APOE
gene interactions at baseline and following change in plasma FA were assessed using adjusted general linear models. At baseline
E4
carriers had higher plasma concentrations of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apo B) compared with
E2
carriers; and higher TC, LDL-C and apo B compared with
E3/E3
. Whilst elevated plasma n-3 polyunsaturated FA (PUFA) was associated with a beneficially lower concentration of apo CIII in
E2
carriers, a high proportion of plasma C16:0 was associated with insulin resistance in
E4
carriers. Following FA intervention, a reduction in plasma long-chain n-3 PUFA was associated with a reduction in apo CII concentration in
E2
carriers. Our novel data suggest that individuals with MetS may benefit from personalized dietary interventions based on
APOE
genotype.</description><subject>45/22</subject><subject>45/23</subject><subject>631/208/212/2130</subject><subject>692/163/2743/2037</subject><subject>692/53/2421</subject><subject>692/700/459/284</subject><subject>82/16</subject><subject>Adult</subject><subject>Aged</subject><subject>Apolipoprotein B</subject><subject>Apolipoprotein C-II - metabolism</subject><subject>Apolipoprotein C-III</subject><subject>Apolipoprotein CII</subject><subject>Apolipoprotein E</subject><subject>Apolipoprotein E4</subject><subject>Apolipoproteins</subject><subject>Apolipoproteins E - genetics</subject><subject>Blood pressure</subject><subject>Cholesterol</subject><subject>Diet</subject><subject>Fatty acids</subject><subject>Fatty Acids - blood</subject><subject>Female</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Insulin</subject><subject>Insulin Resistance</subject><subject>Lipids - analysis</subject><subject>Low density lipoprotein</subject><subject>Male</subject><subject>Metabolic disorders</subject><subject>Metabolic syndrome</subject><subject>Metabolic Syndrome - blood</subject><subject>Metabolic Syndrome - genetics</subject><subject>Metabolic Syndrome - pathology</subject><subject>Middle Aged</subject><subject>multidisciplinary</subject><subject>Polymorphism, Genetic</subject><subject>Polyunsaturated fatty acids</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp1kt9qFDEUxgdRbKl9AS8k4I0XHU0yySS5EZZadaFSwT-3IZM5s80ym4xJRtlH8K3N7tayFQyBc8j5ne8k4auq5wS_JriRbxIjXMkaE1FjLjGt6aPqlGLGa9pQ-vgoP6nOU1rjsjhVjKin1QmVgmFC-Wn1e_H55gqtwIe8nQA5P4wzeAuppGkenUcRkkvZlLMLZKYwuilMMWQopcvlEhnf72JJrA2xd36FckDTaNLGoMHkvC0V16PSM7hxNwHlW0CfIJuuiFn0Zev7GDbwrHoymDHB-V08q769v_p6-bG-vvmwvFxc15YLket24MYSQRRWQgA0mFgCg-QYDDNAmLVtRylTtiWss6otsReCdpZRRTqQzVm1POj2waz1FN3GxK0Oxun9QYgrbWJ2dgQt20YYJctWmIESkqkOupZ2EigWQ1u0Lg5a6RdMc_dA7Z37vtirzbNumoZTXvC3B7ywG-gt-BzN-KDrYcW7W70KPzXnlEnGisCrO4EYfsyQst64ZGEcjYcwJ00UbQhpCdmhL_9B12GOvvxsoXhLBJVKFIoeKBtDShGG-8sQrHc-0wef6eIzvfeZpqXpxfEz7lv-uqoAzd23lJJfQTya_X_ZP66T3os</recordid><startdate>20170724</startdate><enddate>20170724</enddate><creator>Fallaize, Rosalind</creator><creator>Carvalho-Wells, Andrew L.</creator><creator>Tierney, Audrey C.</creator><creator>Marin, Carmen</creator><creator>Kieć-Wilk, Beata</creator><creator>Dembińska-Kieć, Aldona</creator><creator>Drevon, Christian A.</creator><creator>DeFoort, Catherine</creator><creator>Lopez-Miranda, José</creator><creator>Risérus, Ulf</creator><creator>Saris, Wim H.</creator><creator>Blaak, Ellen E.</creator><creator>Roche, Helen M.</creator><creator>Lovegrove, Julie A.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><general>Nature Portfolio</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>ACNBI</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>DF2</scope><scope>ZZAVC</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-3734-6489</orcidid></search><sort><creationdate>20170724</creationdate><title>APOE genotype influences insulin resistance, apolipoprotein CII and CIII according to plasma fatty acid profile in the Metabolic Syndrome</title><author>Fallaize, Rosalind ; Carvalho-Wells, Andrew L. ; Tierney, Audrey C. ; Marin, Carmen ; Kieć-Wilk, Beata ; Dembińska-Kieć, Aldona ; Drevon, Christian A. ; DeFoort, Catherine ; Lopez-Miranda, José ; Risérus, Ulf ; Saris, Wim H. ; Blaak, Ellen E. ; Roche, Helen M. ; Lovegrove, Julie A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c577t-6f5ac17190977ee301c1ef850ea4ae14cc6b2249c614bc96c61d772bc4291be83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>45/22</topic><topic>45/23</topic><topic>631/208/212/2130</topic><topic>692/163/2743/2037</topic><topic>692/53/2421</topic><topic>692/700/459/284</topic><topic>82/16</topic><topic>Adult</topic><topic>Aged</topic><topic>Apolipoprotein B</topic><topic>Apolipoprotein C-II - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SWEPUB Uppsala universitet full text</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SWEPUB Uppsala universitet</collection><collection>SwePub Articles full text</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fallaize, Rosalind</au><au>Carvalho-Wells, Andrew L.</au><au>Tierney, Audrey C.</au><au>Marin, Carmen</au><au>Kieć-Wilk, Beata</au><au>Dembińska-Kieć, Aldona</au><au>Drevon, Christian A.</au><au>DeFoort, Catherine</au><au>Lopez-Miranda, José</au><au>Risérus, Ulf</au><au>Saris, Wim H.</au><au>Blaak, Ellen E.</au><au>Roche, Helen M.</au><au>Lovegrove, Julie A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>APOE genotype influences insulin resistance, apolipoprotein CII and CIII according to plasma fatty acid profile in the Metabolic Syndrome</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2017-07-24</date><risdate>2017</risdate><volume>7</volume><issue>1</issue><spage>6274</spage><epage>10</epage><pages>6274-10</pages><artnum>6274</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Metabolic markers associated with the Metabolic Syndrome (MetS) may be affected by interactions between the
APOE
genotype and plasma fatty acids (FA). In this study, we explored FA-gene interactions between the missense
APOE
polymorphisms and FA status on metabolic markers in MetS. Plasma FA, blood pressure, insulin sensitivity and lipid concentrations were determined at baseline and following a 12-week randomized, controlled, parallel, dietary FA intervention in 442 adults with MetS (LIPGENE study). FA-
APOE
gene interactions at baseline and following change in plasma FA were assessed using adjusted general linear models. At baseline
E4
carriers had higher plasma concentrations of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apo B) compared with
E2
carriers; and higher TC, LDL-C and apo B compared with
E3/E3
. Whilst elevated plasma n-3 polyunsaturated FA (PUFA) was associated with a beneficially lower concentration of apo CIII in
E2
carriers, a high proportion of plasma C16:0 was associated with insulin resistance in
E4
carriers. Following FA intervention, a reduction in plasma long-chain n-3 PUFA was associated with a reduction in apo CII concentration in
E2
carriers. Our novel data suggest that individuals with MetS may benefit from personalized dietary interventions based on
APOE
genotype.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>28740125</pmid><doi>10.1038/s41598-017-05802-2</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-3734-6489</orcidid><oa>free_for_read</oa></addata></record> |
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source | PubMed Central Free; Publicly Available Content (ProQuest); Free Full-Text Journals in Chemistry; Springer Nature - nature.com Journals - Fully Open Access |
subjects | 45/22 45/23 631/208/212/2130 692/163/2743/2037 692/53/2421 692/700/459/284 82/16 Adult Aged Apolipoprotein B Apolipoprotein C-II - metabolism Apolipoprotein C-III Apolipoprotein CII Apolipoprotein E Apolipoprotein E4 Apolipoproteins Apolipoproteins E - genetics Blood pressure Cholesterol Diet Fatty acids Fatty Acids - blood Female Genotype Genotype & phenotype Humanities and Social Sciences Humans Insulin Insulin Resistance Lipids - analysis Low density lipoprotein Male Metabolic disorders Metabolic syndrome Metabolic Syndrome - blood Metabolic Syndrome - genetics Metabolic Syndrome - pathology Middle Aged multidisciplinary Polymorphism, Genetic Polyunsaturated fatty acids Science Science (multidisciplinary) |
title | APOE genotype influences insulin resistance, apolipoprotein CII and CIII according to plasma fatty acid profile in the Metabolic Syndrome |
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