The common insertional polymorphism in the APOC1 promoter is associated with serum apolipoprotein C-I levels in Hispanic children
We examined the effect of APOC1-317insCGTT allele status ( HpaI RFLP, deletion [H1] and insertion [H2] alleles) on serum apolipoprotein (apo) C-I level in 362 Hispanic children in the Columbia University BioMarkers Study. The H2 allele was present in 147 subjects (40.6%). Serum apoC-I was 20% lower...
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creator | Shachter, Neil S. Rabinowitz, Daniel Stohl, Sheldon Conde-Knape, Karin Cohn, Jeffrey S. Deckelbaum, Richard J. Berglund, Lars Shea, Steven |
description | We examined the effect of
APOC1-317insCGTT allele status (
HpaI RFLP, deletion [H1] and insertion [H2] alleles) on serum apolipoprotein (apo) C-I level in 362 Hispanic children in the Columbia University BioMarkers Study. The H2 allele was present in 147 subjects (40.6%). Serum apoC-I was 20% lower in the presence of the H2 allele in
APOE ɛ3/ɛ3 homozygotes (
P
=
0.003) but did not differ by H2 status in ɛ4 carriers. Insufficient numbers of ɛ2 carriers (
N
=
45) were present for analysis. In multivariate analysis in the ɛ3/ɛ3 context, after adjusting for potential covariate effects and familial aggregation, the mean effect of H2/* versus H1/H1 on apoC-I level, was estimated to be 2.15
±
0.55
mg/dl (
P
<
0.0025). Plasma triglyceride level was weakly correlated with serum apoC-I level (Pearson's
r
=
0.17,
P
<
0.001) but was highly correlated with serum apoC-III (Pearson's
r
=
0.74,
P
<
0.0001). Nevertheless, presence of the H2 allele was not significantly associated with serum apoC-III level. Thus, the effect of
APOC1 genotype on serum apoC-I level was not due to apoC-I level serving as a surrogate for triglyceride level. The
APOC1-317insCGTT allele is a commonly polymorphic genetic marker that is associated with serum apoC-I level in the
APOE ɛ3/ɛ3 context. These findings suggest that the mechanism of the previously described association with plasma TG is, at least in part, related to the correlation of the polymorphism with the level of expression of apoC-I. |
doi_str_mv | 10.1016/j.atherosclerosis.2004.10.032 |
format | Article |
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APOC1-317insCGTT allele status (
HpaI RFLP, deletion [H1] and insertion [H2] alleles) on serum apolipoprotein (apo) C-I level in 362 Hispanic children in the Columbia University BioMarkers Study. The H2 allele was present in 147 subjects (40.6%). Serum apoC-I was 20% lower in the presence of the H2 allele in
APOE ɛ3/ɛ3 homozygotes (
P
=
0.003) but did not differ by H2 status in ɛ4 carriers. Insufficient numbers of ɛ2 carriers (
N
=
45) were present for analysis. In multivariate analysis in the ɛ3/ɛ3 context, after adjusting for potential covariate effects and familial aggregation, the mean effect of H2/* versus H1/H1 on apoC-I level, was estimated to be 2.15
±
0.55
mg/dl (
P
<
0.0025). Plasma triglyceride level was weakly correlated with serum apoC-I level (Pearson's
r
=
0.17,
P
<
0.001) but was highly correlated with serum apoC-III (Pearson's
r
=
0.74,
P
<
0.0001). Nevertheless, presence of the H2 allele was not significantly associated with serum apoC-III level. Thus, the effect of
APOC1 genotype on serum apoC-I level was not due to apoC-I level serving as a surrogate for triglyceride level. The
APOC1-317insCGTT allele is a commonly polymorphic genetic marker that is associated with serum apoC-I level in the
APOE ɛ3/ɛ3 context. These findings suggest that the mechanism of the previously described association with plasma TG is, at least in part, related to the correlation of the polymorphism with the level of expression of apoC-I.</description><identifier>ISSN: 0021-9150</identifier><identifier>EISSN: 1879-1484</identifier><identifier>DOI: 10.1016/j.atherosclerosis.2004.10.032</identifier><identifier>PMID: 15777558</identifier><language>eng</language><publisher>Amsterdam: Elsevier Ireland Ltd</publisher><subject>Adolescent ; Apolipoprotein C-I ; Apolipoproteins C ; Apolipoproteins C - blood ; Apolipoproteins C - genetics ; Apolipoproteins E ; Atherosclerosis (general aspects, experimental research) ; Biochemical ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Child ; Coronary heart disease ; Cross-Sectional Studies ; Female ; General and cellular metabolism. Vitamins ; Genetic Markers ; Genetics ; Genotype ; Heart ; Hispanic Americans ; Humans ; Hypertriglyceridemia ; Male ; Medical sciences ; Multivariate Analysis ; Pharmacology. Drug treatments ; Polymorphism, Genetic ; Promoter Regions, Genetic - genetics ; Triglycerides - blood</subject><ispartof>Atherosclerosis, 2005-04, Vol.179 (2), p.387-393</ispartof><rights>2004 Elsevier Ireland Ltd</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-7fce0def7b7957ba4c6c21e7f40dfcc745b0101f050c858c616fc59600a4f4f93</citedby><cites>FETCH-LOGICAL-c417t-7fce0def7b7957ba4c6c21e7f40dfcc745b0101f050c858c616fc59600a4f4f93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.atherosclerosis.2004.10.032$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16611304$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15777558$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shachter, Neil S.</creatorcontrib><creatorcontrib>Rabinowitz, Daniel</creatorcontrib><creatorcontrib>Stohl, Sheldon</creatorcontrib><creatorcontrib>Conde-Knape, Karin</creatorcontrib><creatorcontrib>Cohn, Jeffrey S.</creatorcontrib><creatorcontrib>Deckelbaum, Richard J.</creatorcontrib><creatorcontrib>Berglund, Lars</creatorcontrib><creatorcontrib>Shea, Steven</creatorcontrib><title>The common insertional polymorphism in the APOC1 promoter is associated with serum apolipoprotein C-I levels in Hispanic children</title><title>Atherosclerosis</title><addtitle>Atherosclerosis</addtitle><description>We examined the effect of
APOC1-317insCGTT allele status (
HpaI RFLP, deletion [H1] and insertion [H2] alleles) on serum apolipoprotein (apo) C-I level in 362 Hispanic children in the Columbia University BioMarkers Study. The H2 allele was present in 147 subjects (40.6%). Serum apoC-I was 20% lower in the presence of the H2 allele in
APOE ɛ3/ɛ3 homozygotes (
P
=
0.003) but did not differ by H2 status in ɛ4 carriers. Insufficient numbers of ɛ2 carriers (
N
=
45) were present for analysis. In multivariate analysis in the ɛ3/ɛ3 context, after adjusting for potential covariate effects and familial aggregation, the mean effect of H2/* versus H1/H1 on apoC-I level, was estimated to be 2.15
±
0.55
mg/dl (
P
<
0.0025). Plasma triglyceride level was weakly correlated with serum apoC-I level (Pearson's
r
=
0.17,
P
<
0.001) but was highly correlated with serum apoC-III (Pearson's
r
=
0.74,
P
<
0.0001). Nevertheless, presence of the H2 allele was not significantly associated with serum apoC-III level. Thus, the effect of
APOC1 genotype on serum apoC-I level was not due to apoC-I level serving as a surrogate for triglyceride level. The
APOC1-317insCGTT allele is a commonly polymorphic genetic marker that is associated with serum apoC-I level in the
APOE ɛ3/ɛ3 context. These findings suggest that the mechanism of the previously described association with plasma TG is, at least in part, related to the correlation of the polymorphism with the level of expression of apoC-I.</description><subject>Adolescent</subject><subject>Apolipoprotein C-I</subject><subject>Apolipoproteins C</subject><subject>Apolipoproteins C - blood</subject><subject>Apolipoproteins C - genetics</subject><subject>Apolipoproteins E</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biochemical</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Child</subject><subject>Coronary heart disease</subject><subject>Cross-Sectional Studies</subject><subject>Female</subject><subject>General and cellular metabolism. Vitamins</subject><subject>Genetic Markers</subject><subject>Genetics</subject><subject>Genotype</subject><subject>Heart</subject><subject>Hispanic Americans</subject><subject>Humans</subject><subject>Hypertriglyceridemia</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Multivariate Analysis</subject><subject>Pharmacology. Drug treatments</subject><subject>Polymorphism, Genetic</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Triglycerides - blood</subject><issn>0021-9150</issn><issn>1879-1484</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkTFv2zAQhYmgQeOm_QsBl3STS8qkKA0dAqNNAgRIhnQm6NMRokGJKkmnyJh_Xgo2WqBTF3K47909vEfINWdrznjzZb82ecAYEvjldWldMybKbM029RlZ8VZ1FReteEdWjNW86rhkF-RDSntWQMXb9-SCS6WUlO2KvD0PSCGMY5iomxLG7MJkPJ2Dfx1DnAeXxjKg5Sa9eXrccjrHMIaMkbpETUoBnMnY018uD7ToDyM1RezmUMCMRbqt7qnHF_RpWXTn0mwmBxQG5_uI00dybo1P-On0X5If3789b--qh8fb--3NQwWCq1wpC8h6tGqnOql2RkADNUdlBestgBJyx0pAlkkGrWyh4Y0F2TWMGWGF7TaX5PNxb_H184Ap69ElQO_NhOGQdKNkLVslCvj1CELJN0W0eo5uNPFVc6aXDvRe_9OBXjpYxqWDor86HTrsRuz_qk-hF-D6BJgExttoJig7_nBNw_mGLUZuj1yJDl8cRp3A4QTYu4iQdR_cf1r6DacssbY</recordid><startdate>20050401</startdate><enddate>20050401</enddate><creator>Shachter, Neil S.</creator><creator>Rabinowitz, Daniel</creator><creator>Stohl, Sheldon</creator><creator>Conde-Knape, Karin</creator><creator>Cohn, Jeffrey S.</creator><creator>Deckelbaum, Richard J.</creator><creator>Berglund, Lars</creator><creator>Shea, Steven</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>20050401</creationdate><title>The common insertional polymorphism in the APOC1 promoter is associated with serum apolipoprotein C-I levels in Hispanic children</title><author>Shachter, Neil S. ; Rabinowitz, Daniel ; Stohl, Sheldon ; Conde-Knape, Karin ; Cohn, Jeffrey S. ; Deckelbaum, Richard J. ; Berglund, Lars ; Shea, Steven</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-7fce0def7b7957ba4c6c21e7f40dfcc745b0101f050c858c616fc59600a4f4f93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adolescent</topic><topic>Apolipoprotein C-I</topic><topic>Apolipoproteins C</topic><topic>Apolipoproteins C - blood</topic><topic>Apolipoproteins C - genetics</topic><topic>Apolipoproteins E</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biochemical</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Child</topic><topic>Coronary heart disease</topic><topic>Cross-Sectional Studies</topic><topic>Female</topic><topic>General and cellular metabolism. Vitamins</topic><topic>Genetic Markers</topic><topic>Genetics</topic><topic>Genotype</topic><topic>Heart</topic><topic>Hispanic Americans</topic><topic>Humans</topic><topic>Hypertriglyceridemia</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Multivariate Analysis</topic><topic>Pharmacology. Drug treatments</topic><topic>Polymorphism, Genetic</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Triglycerides - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shachter, Neil S.</creatorcontrib><creatorcontrib>Rabinowitz, Daniel</creatorcontrib><creatorcontrib>Stohl, Sheldon</creatorcontrib><creatorcontrib>Conde-Knape, Karin</creatorcontrib><creatorcontrib>Cohn, Jeffrey S.</creatorcontrib><creatorcontrib>Deckelbaum, Richard J.</creatorcontrib><creatorcontrib>Berglund, Lars</creatorcontrib><creatorcontrib>Shea, Steven</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>Shachter, Neil S.</au><au>Rabinowitz, Daniel</au><au>Stohl, Sheldon</au><au>Conde-Knape, Karin</au><au>Cohn, Jeffrey S.</au><au>Deckelbaum, Richard J.</au><au>Berglund, Lars</au><au>Shea, Steven</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The common insertional polymorphism in the APOC1 promoter is associated with serum apolipoprotein C-I levels in Hispanic children</atitle><jtitle>Atherosclerosis</jtitle><addtitle>Atherosclerosis</addtitle><date>2005-04-01</date><risdate>2005</risdate><volume>179</volume><issue>2</issue><spage>387</spage><epage>393</epage><pages>387-393</pages><issn>0021-9150</issn><eissn>1879-1484</eissn><abstract>We examined the effect of
APOC1-317insCGTT allele status (
HpaI RFLP, deletion [H1] and insertion [H2] alleles) on serum apolipoprotein (apo) C-I level in 362 Hispanic children in the Columbia University BioMarkers Study. The H2 allele was present in 147 subjects (40.6%). Serum apoC-I was 20% lower in the presence of the H2 allele in
APOE ɛ3/ɛ3 homozygotes (
P
=
0.003) but did not differ by H2 status in ɛ4 carriers. Insufficient numbers of ɛ2 carriers (
N
=
45) were present for analysis. In multivariate analysis in the ɛ3/ɛ3 context, after adjusting for potential covariate effects and familial aggregation, the mean effect of H2/* versus H1/H1 on apoC-I level, was estimated to be 2.15
±
0.55
mg/dl (
P
<
0.0025). Plasma triglyceride level was weakly correlated with serum apoC-I level (Pearson's
r
=
0.17,
P
<
0.001) but was highly correlated with serum apoC-III (Pearson's
r
=
0.74,
P
<
0.0001). Nevertheless, presence of the H2 allele was not significantly associated with serum apoC-III level. Thus, the effect of
APOC1 genotype on serum apoC-I level was not due to apoC-I level serving as a surrogate for triglyceride level. The
APOC1-317insCGTT allele is a commonly polymorphic genetic marker that is associated with serum apoC-I level in the
APOE ɛ3/ɛ3 context. These findings suggest that the mechanism of the previously described association with plasma TG is, at least in part, related to the correlation of the polymorphism with the level of expression of apoC-I.</abstract><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>15777558</pmid><doi>10.1016/j.atherosclerosis.2004.10.032</doi><tpages>7</tpages></addata></record> |
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language | eng |
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source | MEDLINE; Elsevier ScienceDirect Journals Complete |
subjects | Adolescent Apolipoprotein C-I Apolipoproteins C Apolipoproteins C - blood Apolipoproteins C - genetics Apolipoproteins E Atherosclerosis (general aspects, experimental research) Biochemical Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Child Coronary heart disease Cross-Sectional Studies Female General and cellular metabolism. Vitamins Genetic Markers Genetics Genotype Heart Hispanic Americans Humans Hypertriglyceridemia Male Medical sciences Multivariate Analysis Pharmacology. Drug treatments Polymorphism, Genetic Promoter Regions, Genetic - genetics Triglycerides - blood |
title | The common insertional polymorphism in the APOC1 promoter is associated with serum apolipoprotein C-I levels in Hispanic children |
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