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Interactive effects of C-reactive protein levels on the association between APOE variants and triglyceride levels in a Taiwanese population
Apolipoprotein E (APOE) plays a major role in lipid metabolism and inflammation. However, the association between APOE gene polymorphisms and serum triglyceride levels remains controversial. We tested the effects of APOE variants on triglyceride levels and their interactions with the inflammatory ma...
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Published in: | Lipids in health and disease 2016-05, Vol.15 (94), p.94-94, Article 94 |
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description | Apolipoprotein E (APOE) plays a major role in lipid metabolism and inflammation. However, the association between APOE gene polymorphisms and serum triglyceride levels remains controversial. We tested the effects of APOE variants on triglyceride levels and their interactions with the inflammatory marker C-reactive protein (CRP) in a Taiwanese population.
Two APOE single nucleotide polymorphisms (SNPs) rs429358 and rs7412 were genotyped by TaqMan Assay using real time PCR in 595 healthy subjects attending the clinic for routine visits.
After adjustment for clinical covariates, subjects carrying the rs429358-TT genotype and non-ε4 alleles were found to have higher CRP levels, whereas those with rs7412-CC genotype and non-ε2 alleles had significantly higher total and low-density lipoprotein cholesterol levels (all P < 0.01). Using subgroup and interaction analyses, we observed significantly lower triglyceride levels in subjects carrying the rs429358-TT genotype and non-ε4 alleles in the low CRP group (P = 2.71 × 10(-4) and P = 4.32 × 10(-4), respectively), but not in those in the high CRP group (interaction P = 0.013 and 0.045, respectively). In addition, multivariate stepwise linear regression analysis showed that subjects carrying the rs429358-TT genotype and non-ε4 alleles with low CRP levels had significantly lower triglyceride levels (P < 0.001 and P < 0.001, respectively). In addition, when combined with the risk alleles of GCKR, APOA5 and LPL gene variants, we observed that triglyceride levels increased significantly with the number of risk alleles (P = 2.9 × 10(-12)).
The combination of SNPs and ε alleles at the APOE locus is involved in managing lipid and CRP levels in the Taiwanese population. APOE polymorphisms interact with CRP to regulate triglyceride levels, thus triglyceride concentration is influenced by both the genetic background of the APOE locus and the inflammatory status of a subject. |
doi_str_mv | 10.1186/s12944-016-0262-z |
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Two APOE single nucleotide polymorphisms (SNPs) rs429358 and rs7412 were genotyped by TaqMan Assay using real time PCR in 595 healthy subjects attending the clinic for routine visits.
After adjustment for clinical covariates, subjects carrying the rs429358-TT genotype and non-ε4 alleles were found to have higher CRP levels, whereas those with rs7412-CC genotype and non-ε2 alleles had significantly higher total and low-density lipoprotein cholesterol levels (all P < 0.01). Using subgroup and interaction analyses, we observed significantly lower triglyceride levels in subjects carrying the rs429358-TT genotype and non-ε4 alleles in the low CRP group (P = 2.71 × 10(-4) and P = 4.32 × 10(-4), respectively), but not in those in the high CRP group (interaction P = 0.013 and 0.045, respectively). In addition, multivariate stepwise linear regression analysis showed that subjects carrying the rs429358-TT genotype and non-ε4 alleles with low CRP levels had significantly lower triglyceride levels (P < 0.001 and P < 0.001, respectively). In addition, when combined with the risk alleles of GCKR, APOA5 and LPL gene variants, we observed that triglyceride levels increased significantly with the number of risk alleles (P = 2.9 × 10(-12)).
The combination of SNPs and ε alleles at the APOE locus is involved in managing lipid and CRP levels in the Taiwanese population. APOE polymorphisms interact with CRP to regulate triglyceride levels, thus triglyceride concentration is influenced by both the genetic background of the APOE locus and the inflammatory status of a subject.</description><identifier>ISSN: 1476-511X</identifier><identifier>EISSN: 1476-511X</identifier><identifier>DOI: 10.1186/s12944-016-0262-z</identifier><identifier>PMID: 27177774</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Adaptor Proteins, Signal Transducing - genetics ; Adult ; Analysis ; Apolipoprotein A-V - genetics ; Apolipoproteins E - genetics ; Asian Continental Ancestry Group - genetics ; Biomarkers - blood ; C-reactive protein ; C-Reactive Protein - genetics ; C-Reactive Protein - metabolism ; Female ; Health aspects ; Humans ; Inflammation - genetics ; Inflammation - metabolism ; Lipid metabolism ; Lipids - blood ; Lipids - genetics ; Lipoprotein Lipase - genetics ; Low density lipoproteins ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Single nucleotide polymorphisms ; Taiwan ; Triglycerides - blood ; Triglycerides - genetics</subject><ispartof>Lipids in health and disease, 2016-05, Vol.15 (94), p.94-94, Article 94</ispartof><rights>COPYRIGHT 2016 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2016</rights><rights>Wu et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-817c85585b433cde1ef77de72ef835c2a5720ba74d457ea881fb1bdfb28790713</citedby><cites>FETCH-LOGICAL-c494t-817c85585b433cde1ef77de72ef835c2a5720ba74d457ea881fb1bdfb28790713</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4866423/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1804470886?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27177774$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Semon</creatorcontrib><creatorcontrib>Hsu, Lung-An</creatorcontrib><creatorcontrib>Teng, Ming-Sheng</creatorcontrib><creatorcontrib>Lin, Jeng-Feng</creatorcontrib><creatorcontrib>Chou, Hsin-Hua</creatorcontrib><creatorcontrib>Lee, Ming-Cheng</creatorcontrib><creatorcontrib>Wu, Yi-Ming</creatorcontrib><creatorcontrib>Su, Cheng-Wen</creatorcontrib><creatorcontrib>Ko, Yu-Lin</creatorcontrib><title>Interactive effects of C-reactive protein levels on the association between APOE variants and triglyceride levels in a Taiwanese population</title><title>Lipids in health and disease</title><addtitle>Lipids Health Dis</addtitle><description>Apolipoprotein E (APOE) plays a major role in lipid metabolism and inflammation. However, the association between APOE gene polymorphisms and serum triglyceride levels remains controversial. We tested the effects of APOE variants on triglyceride levels and their interactions with the inflammatory marker C-reactive protein (CRP) in a Taiwanese population.
Two APOE single nucleotide polymorphisms (SNPs) rs429358 and rs7412 were genotyped by TaqMan Assay using real time PCR in 595 healthy subjects attending the clinic for routine visits.
After adjustment for clinical covariates, subjects carrying the rs429358-TT genotype and non-ε4 alleles were found to have higher CRP levels, whereas those with rs7412-CC genotype and non-ε2 alleles had significantly higher total and low-density lipoprotein cholesterol levels (all P < 0.01). Using subgroup and interaction analyses, we observed significantly lower triglyceride levels in subjects carrying the rs429358-TT genotype and non-ε4 alleles in the low CRP group (P = 2.71 × 10(-4) and P = 4.32 × 10(-4), respectively), but not in those in the high CRP group (interaction P = 0.013 and 0.045, respectively). In addition, multivariate stepwise linear regression analysis showed that subjects carrying the rs429358-TT genotype and non-ε4 alleles with low CRP levels had significantly lower triglyceride levels (P < 0.001 and P < 0.001, respectively). In addition, when combined with the risk alleles of GCKR, APOA5 and LPL gene variants, we observed that triglyceride levels increased significantly with the number of risk alleles (P = 2.9 × 10(-12)).
The combination of SNPs and ε alleles at the APOE locus is involved in managing lipid and CRP levels in the Taiwanese population. APOE polymorphisms interact with CRP to regulate triglyceride levels, thus triglyceride concentration is influenced by both the genetic background of the APOE locus and the inflammatory status of a subject.</description><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adult</subject><subject>Analysis</subject><subject>Apolipoprotein A-V - genetics</subject><subject>Apolipoproteins E - genetics</subject><subject>Asian Continental Ancestry Group - genetics</subject><subject>Biomarkers - blood</subject><subject>C-reactive protein</subject><subject>C-Reactive Protein - genetics</subject><subject>C-Reactive Protein - metabolism</subject><subject>Female</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Inflammation - genetics</subject><subject>Inflammation - metabolism</subject><subject>Lipid metabolism</subject><subject>Lipids - blood</subject><subject>Lipids - genetics</subject><subject>Lipoprotein Lipase - genetics</subject><subject>Low density lipoproteins</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Single nucleotide polymorphisms</subject><subject>Taiwan</subject><subject>Triglycerides - blood</subject><subject>Triglycerides - genetics</subject><issn>1476-511X</issn><issn>1476-511X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNptkkFPHCEYhidNm2ptf0AvDUkvvYwFhgHm0mSz0WpiYg-a9EYY5mPFzMIWmDX6F_qnZd3VaiMcgI_3fchH3qr6TPAhIZJ_T4R2jNWY8BpTTuu7N9U-YYLXLSG_3z7b71UfUrrGmGLB-ftqjwoiymD71d9TnyFqk90aEFgLJicULJrXEXbVVQwZnEcjrGEslx7lK0A6pWCczq6ce8g3AB7Nfp0fobWOTvtC0X5AObrFeGsgugEeAQWl0YV2N9pDKviwmsYHzsfqndVjgk-79aC6PD66mJ_UZ-c_T-ezs9qwjuVaEmFk28q2Z01jBiBghRhAULCyaQ3VraC414INrBWgpSS2J_1geypFhwVpDqofW-5q6pcwGPA56lGtolvqeKuCdurljXdXahHWiknOGW0K4NsOEMOfCVJWS5cMjGPpKExJESE71vEO0yL9-p_0OkzRl_YUkZgxgaXk_1QLPYJy3obyrtlA1Yy1jRSY4baoDl9RlTnA0pngwbpSf2EgW4OJIaUI9qlHgtUmQWqbIFUSpDYJUnfF8-X55zw5HiPT3AMZQ8Oa</recordid><startdate>20160513</startdate><enddate>20160513</enddate><creator>Wu, Semon</creator><creator>Hsu, Lung-An</creator><creator>Teng, Ming-Sheng</creator><creator>Lin, Jeng-Feng</creator><creator>Chou, Hsin-Hua</creator><creator>Lee, Ming-Cheng</creator><creator>Wu, Yi-Ming</creator><creator>Su, Cheng-Wen</creator><creator>Ko, Yu-Lin</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><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>88E</scope><scope>8FD</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>FR3</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>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160513</creationdate><title>Interactive effects of C-reactive protein levels on the association between APOE variants and triglyceride levels in a Taiwanese population</title><author>Wu, Semon ; Hsu, Lung-An ; Teng, Ming-Sheng ; Lin, Jeng-Feng ; Chou, Hsin-Hua ; Lee, Ming-Cheng ; Wu, Yi-Ming ; Su, Cheng-Wen ; Ko, Yu-Lin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-817c85585b433cde1ef77de72ef835c2a5720ba74d457ea881fb1bdfb28790713</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adult</topic><topic>Analysis</topic><topic>Apolipoprotein A-V - genetics</topic><topic>Apolipoproteins E - genetics</topic><topic>Asian Continental Ancestry Group - genetics</topic><topic>Biomarkers - blood</topic><topic>C-reactive protein</topic><topic>C-Reactive Protein - genetics</topic><topic>C-Reactive Protein - metabolism</topic><topic>Female</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Inflammation - genetics</topic><topic>Inflammation - metabolism</topic><topic>Lipid metabolism</topic><topic>Lipids - blood</topic><topic>Lipids - genetics</topic><topic>Lipoprotein Lipase - genetics</topic><topic>Low density lipoproteins</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Single nucleotide polymorphisms</topic><topic>Taiwan</topic><topic>Triglycerides - blood</topic><topic>Triglycerides - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Semon</creatorcontrib><creatorcontrib>Hsu, Lung-An</creatorcontrib><creatorcontrib>Teng, Ming-Sheng</creatorcontrib><creatorcontrib>Lin, Jeng-Feng</creatorcontrib><creatorcontrib>Chou, Hsin-Hua</creatorcontrib><creatorcontrib>Lee, Ming-Cheng</creatorcontrib><creatorcontrib>Wu, Yi-Ming</creatorcontrib><creatorcontrib>Su, Cheng-Wen</creatorcontrib><creatorcontrib>Ko, Yu-Lin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Biological Science Journals</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Lipids in health and disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Semon</au><au>Hsu, Lung-An</au><au>Teng, Ming-Sheng</au><au>Lin, Jeng-Feng</au><au>Chou, Hsin-Hua</au><au>Lee, Ming-Cheng</au><au>Wu, Yi-Ming</au><au>Su, Cheng-Wen</au><au>Ko, Yu-Lin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interactive effects of C-reactive protein levels on the association between APOE variants and triglyceride levels in a Taiwanese population</atitle><jtitle>Lipids in health and disease</jtitle><addtitle>Lipids Health Dis</addtitle><date>2016-05-13</date><risdate>2016</risdate><volume>15</volume><issue>94</issue><spage>94</spage><epage>94</epage><pages>94-94</pages><artnum>94</artnum><issn>1476-511X</issn><eissn>1476-511X</eissn><abstract>Apolipoprotein E (APOE) plays a major role in lipid metabolism and inflammation. However, the association between APOE gene polymorphisms and serum triglyceride levels remains controversial. We tested the effects of APOE variants on triglyceride levels and their interactions with the inflammatory marker C-reactive protein (CRP) in a Taiwanese population.
Two APOE single nucleotide polymorphisms (SNPs) rs429358 and rs7412 were genotyped by TaqMan Assay using real time PCR in 595 healthy subjects attending the clinic for routine visits.
After adjustment for clinical covariates, subjects carrying the rs429358-TT genotype and non-ε4 alleles were found to have higher CRP levels, whereas those with rs7412-CC genotype and non-ε2 alleles had significantly higher total and low-density lipoprotein cholesterol levels (all P < 0.01). Using subgroup and interaction analyses, we observed significantly lower triglyceride levels in subjects carrying the rs429358-TT genotype and non-ε4 alleles in the low CRP group (P = 2.71 × 10(-4) and P = 4.32 × 10(-4), respectively), but not in those in the high CRP group (interaction P = 0.013 and 0.045, respectively). In addition, multivariate stepwise linear regression analysis showed that subjects carrying the rs429358-TT genotype and non-ε4 alleles with low CRP levels had significantly lower triglyceride levels (P < 0.001 and P < 0.001, respectively). In addition, when combined with the risk alleles of GCKR, APOA5 and LPL gene variants, we observed that triglyceride levels increased significantly with the number of risk alleles (P = 2.9 × 10(-12)).
The combination of SNPs and ε alleles at the APOE locus is involved in managing lipid and CRP levels in the Taiwanese population. APOE polymorphisms interact with CRP to regulate triglyceride levels, thus triglyceride concentration is influenced by both the genetic background of the APOE locus and the inflammatory status of a subject.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>27177774</pmid><doi>10.1186/s12944-016-0262-z</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adaptor Proteins, Signal Transducing - genetics Adult Analysis Apolipoprotein A-V - genetics Apolipoproteins E - genetics Asian Continental Ancestry Group - genetics Biomarkers - blood C-reactive protein C-Reactive Protein - genetics C-Reactive Protein - metabolism Female Health aspects Humans Inflammation - genetics Inflammation - metabolism Lipid metabolism Lipids - blood Lipids - genetics Lipoprotein Lipase - genetics Low density lipoproteins Male Middle Aged Polymorphism, Single Nucleotide Single nucleotide polymorphisms Taiwan Triglycerides - blood Triglycerides - genetics |
title | Interactive effects of C-reactive protein levels on the association between APOE variants and triglyceride levels in a Taiwanese population |
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