Association of the A/T54 polymorphism in the intestinal fatty acid binding protein with variations in plasma lipids in The Framingham Offspring Study

We investigated the potential role of the genetic variation at the intestinal fatty acid binding protein gene ( FABP2) in influencing lipid levels in a representative sample of the Framingham Offspring Study participants ( n=1930). In men, the T54 allele was associated with significantly higher LDL-...

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Veröffentlicht in:Atherosclerosis 2001-12, Vol.159 (2), p.417-424
Hauptverfasser: Galluzzi, Jennifer R, Cupples, L.Adrienne, Otvos, James D, Wilson, Peter W.F, Schaefer, Ernst J, Ordovas, Jose M
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container_end_page 424
container_issue 2
container_start_page 417
container_title Atherosclerosis
container_volume 159
creator Galluzzi, Jennifer R
Cupples, L.Adrienne
Otvos, James D
Wilson, Peter W.F
Schaefer, Ernst J
Ordovas, Jose M
description We investigated the potential role of the genetic variation at the intestinal fatty acid binding protein gene ( FABP2) in influencing lipid levels in a representative sample of the Framingham Offspring Study participants ( n=1930). In men, the T54 allele was associated with significantly higher LDL-cholesterol (3.47±0.83 vs 3.36±0.83 mmol/l; P
doi_str_mv 10.1016/S0021-9150(01)00517-2
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In men, the T54 allele was associated with significantly higher LDL-cholesterol (3.47±0.83 vs 3.36±0.83 mmol/l; P&lt;0.047), and ApoB (1.04±0.23 vs 1.01±0.24 g/l; P&lt;0.020) after adjustment for familial relationship, age, BMI, smoking, alcohol intake and the use of beta-blockers compared with the A54 allele. This relationship with ApoB continued to be significant after adjustment for APOE genotype ( P&lt;0.034). In women, the T54 allele was associated with significantly higher total-cholesterol (5.32±1.01 vs 5.17±0.98 mmol/l; P&lt;0.049) and LDL-cholesterol (3.31±0.93 vs 3.18±0.85 mmol/l; P&lt;0.023) after adjustment for covariates and menopausal status, estrogen therapy and APOE genotype. In men, the T54 allele was associated with significantly higher levels of small VLDL and lower levels of large HDL. Moreover, there was no significant relationship between FABP2 alleles and lipoprotein diameter or the prevalence of coronary heart disease in both genders. 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In men, the T54 allele was associated with significantly higher LDL-cholesterol (3.47±0.83 vs 3.36±0.83 mmol/l; P&lt;0.047), and ApoB (1.04±0.23 vs 1.01±0.24 g/l; P&lt;0.020) after adjustment for familial relationship, age, BMI, smoking, alcohol intake and the use of beta-blockers compared with the A54 allele. This relationship with ApoB continued to be significant after adjustment for APOE genotype ( P&lt;0.034). In women, the T54 allele was associated with significantly higher total-cholesterol (5.32±1.01 vs 5.17±0.98 mmol/l; P&lt;0.049) and LDL-cholesterol (3.31±0.93 vs 3.18±0.85 mmol/l; P&lt;0.023) after adjustment for covariates and menopausal status, estrogen therapy and APOE genotype. In men, the T54 allele was associated with significantly higher levels of small VLDL and lower levels of large HDL. Moreover, there was no significant relationship between FABP2 alleles and lipoprotein diameter or the prevalence of coronary heart disease in both genders. Our data are consistent with the T54 IFABP increasing the flux of lipids through the enterocyte leading to an increase in chylomicron secretion.</description><subject>Age Distribution</subject><subject>Aged</subject><subject>Alleles</subject><subject>Apolipoproteins - blood</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Carrier Proteins - genetics</subject><subject>Cholesterol</subject><subject>Cohort Studies</subject><subject>Coronary Artery Disease - epidemiology</subject><subject>Coronary Artery Disease - genetics</subject><subject>Coronary heart disease</subject><subject>FABP2</subject><subject>Fatty Acid-Binding Protein 7</subject><subject>Fatty Acid-Binding Proteins</subject><subject>Fatty Acids - metabolism</subject><subject>Female</subject><subject>Framingham</subject><subject>Genetic Predisposition to Disease - epidemiology</subject><subject>Genetic Variation</subject><subject>Heart</subject><subject>Humans</subject><subject>Incidence</subject><subject>Lipids - blood</subject><subject>Lipoproteins - blood</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neoplasm Proteins</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Probability</subject><subject>Prospective Studies</subject><subject>Risk Factors</subject><subject>Sex Distribution</subject><subject>Tumor Suppressor Proteins</subject><issn>0021-9150</issn><issn>1879-1484</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFu1DAURS0EokPhE0DegGAR6uc4iWeFRhUFpEpddFhbjmMzDyV2sD1F8yH8L87MiC5ZWbLPvb7vXUJeA_sIDNqre8Y4VGto2HsGHxhroKv4E7IC2a0rEFI8Jat_yAV5kdJPxpjoQD4nFwBdzSTnK_Jnk1IwqDMGT4OjeWfp5mrbCDqH8TCFOO8wTRT98QV9timj1yN1OucD1QYH2qMf0P-gcwzZFvI35h190PHkmhbxPOo0aTrijMPxYlvcbqKeim6nJ3rnXJrjYnKf98PhJXnm9Jjsq_N5Sb7ffN5ef61u7758u97cVqZeQ66c7IxprOCtNaav60b2fWOsE63rXessay1vXN25VvR912jB60FKBr3Ug2kB6kvy7uRbov_al9HUhMnYcdTehn1SHa-hFbIuYHMCTQwpRetUSTvpeFDA1NKHOvahlmUrBurYh-JF9-b8wb6f7PCoOhdQgLdnQCejRxe1N5geOQEg-XrhPp04W9bxgDaqZNB6YweM1mQ1BPxPlL_prqoB</recordid><startdate>20011201</startdate><enddate>20011201</enddate><creator>Galluzzi, Jennifer R</creator><creator>Cupples, L.Adrienne</creator><creator>Otvos, James D</creator><creator>Wilson, Peter W.F</creator><creator>Schaefer, Ernst J</creator><creator>Ordovas, Jose M</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</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>7X8</scope></search><sort><creationdate>20011201</creationdate><title>Association of the A/T54 polymorphism in the intestinal fatty acid binding protein with variations in plasma lipids in The Framingham Offspring Study</title><author>Galluzzi, Jennifer R ; Cupples, L.Adrienne ; Otvos, James D ; Wilson, Peter W.F ; Schaefer, Ernst J ; Ordovas, Jose M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-f87cc5e426eccb3358bb5cef46fbf6fe06e25f37f64bb75a423d8801b8adc6113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Age Distribution</topic><topic>Aged</topic><topic>Alleles</topic><topic>Apolipoproteins - blood</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Carrier Proteins - genetics</topic><topic>Cholesterol</topic><topic>Cohort Studies</topic><topic>Coronary Artery Disease - epidemiology</topic><topic>Coronary Artery Disease - genetics</topic><topic>Coronary heart disease</topic><topic>FABP2</topic><topic>Fatty Acid-Binding Protein 7</topic><topic>Fatty Acid-Binding Proteins</topic><topic>Fatty Acids - metabolism</topic><topic>Female</topic><topic>Framingham</topic><topic>Genetic Predisposition to Disease - epidemiology</topic><topic>Genetic Variation</topic><topic>Heart</topic><topic>Humans</topic><topic>Incidence</topic><topic>Lipids - blood</topic><topic>Lipoproteins - blood</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neoplasm Proteins</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Probability</topic><topic>Prospective Studies</topic><topic>Risk Factors</topic><topic>Sex Distribution</topic><topic>Tumor Suppressor Proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Galluzzi, Jennifer R</creatorcontrib><creatorcontrib>Cupples, L.Adrienne</creatorcontrib><creatorcontrib>Otvos, James D</creatorcontrib><creatorcontrib>Wilson, Peter W.F</creatorcontrib><creatorcontrib>Schaefer, Ernst J</creatorcontrib><creatorcontrib>Ordovas, Jose M</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Atherosclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Galluzzi, Jennifer R</au><au>Cupples, L.Adrienne</au><au>Otvos, James D</au><au>Wilson, Peter W.F</au><au>Schaefer, Ernst J</au><au>Ordovas, Jose M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of the A/T54 polymorphism in the intestinal fatty acid binding protein with variations in plasma lipids in The Framingham Offspring Study</atitle><jtitle>Atherosclerosis</jtitle><addtitle>Atherosclerosis</addtitle><date>2001-12-01</date><risdate>2001</risdate><volume>159</volume><issue>2</issue><spage>417</spage><epage>424</epage><pages>417-424</pages><issn>0021-9150</issn><eissn>1879-1484</eissn><abstract>We investigated the potential role of the genetic variation at the intestinal fatty acid binding protein gene ( FABP2) in influencing lipid levels in a representative sample of the Framingham Offspring Study participants ( n=1930). In men, the T54 allele was associated with significantly higher LDL-cholesterol (3.47±0.83 vs 3.36±0.83 mmol/l; P&lt;0.047), and ApoB (1.04±0.23 vs 1.01±0.24 g/l; P&lt;0.020) after adjustment for familial relationship, age, BMI, smoking, alcohol intake and the use of beta-blockers compared with the A54 allele. This relationship with ApoB continued to be significant after adjustment for APOE genotype ( P&lt;0.034). In women, the T54 allele was associated with significantly higher total-cholesterol (5.32±1.01 vs 5.17±0.98 mmol/l; P&lt;0.049) and LDL-cholesterol (3.31±0.93 vs 3.18±0.85 mmol/l; P&lt;0.023) after adjustment for covariates and menopausal status, estrogen therapy and APOE genotype. In men, the T54 allele was associated with significantly higher levels of small VLDL and lower levels of large HDL. Moreover, there was no significant relationship between FABP2 alleles and lipoprotein diameter or the prevalence of coronary heart disease in both genders. Our data are consistent with the T54 IFABP increasing the flux of lipids through the enterocyte leading to an increase in chylomicron secretion.</abstract><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>11730822</pmid><doi>10.1016/S0021-9150(01)00517-2</doi><tpages>8</tpages></addata></record>
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subjects Age Distribution
Aged
Alleles
Apolipoproteins - blood
Biological and medical sciences
Cardiology. Vascular system
Carrier Proteins - genetics
Cholesterol
Cohort Studies
Coronary Artery Disease - epidemiology
Coronary Artery Disease - genetics
Coronary heart disease
FABP2
Fatty Acid-Binding Protein 7
Fatty Acid-Binding Proteins
Fatty Acids - metabolism
Female
Framingham
Genetic Predisposition to Disease - epidemiology
Genetic Variation
Heart
Humans
Incidence
Lipids - blood
Lipoproteins - blood
Male
Medical sciences
Middle Aged
Neoplasm Proteins
Polymorphism
Polymorphism, Genetic
Probability
Prospective Studies
Risk Factors
Sex Distribution
Tumor Suppressor Proteins
title Association of the A/T54 polymorphism in the intestinal fatty acid binding protein with variations in plasma lipids in The Framingham Offspring Study
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