Peroxisome Proliferator-Activated Receptor α L162V Polymorphism in Nonalcoholic Steatohepatitis and Genotype 1 Hepatitis C Virus-Related Liver Steatosis
BackgroundPeroxisome proliferator-activated receptor α (PPARα) plays important roles in lipid metabolism. A recently discovered L162V polymorphism of the PPARα gene is associated with enhanced transcriptional activity. In this study, the frequency of L162V was investigated in nonalcoholic steatohepa...
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creator | Verdi, Hasibe Sare Koytak, Elif Önder, Oğuz Arslan Ergül, Ayça Cinar, Kubilay Idilman, Ramazan Erden, Esra Mithat Bozdayi, Abdurrahman Yurdaydin, Cihan Uzunalimoglu, Özden Bozkaya, Hakan |
description | BackgroundPeroxisome proliferator-activated receptor α (PPARα) plays important roles in lipid metabolism. A recently discovered L162V polymorphism of the PPARα gene is associated with enhanced transcriptional activity. In this study, the frequency of L162V was investigated in nonalcoholic steatohepatitis (NASH) and genotype 1 hepatitis C virus (HCV)-related liver steatosis.MethodsSeventy-two NASH and 141 HCV-infected patients (54 with steatosis, 87 without steatosis) and 119 healthy controls were included. L162V polymorphism of the PPARα gene was analyzed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP).ResultsPCR and RFLP analysis of the related gene segment was successful in 93%, 96%, and 100% of NASH and HCV-infected patients and controls, respectively. The frequency of the L162V polymorphism was similar in the NASH and HCV-infected patients and controls (5.9%, 3.6%, and 2.5%, respectively). No difference in the frequency of this polymorphism was observed in HCV-infected patients with or without significant liver steatosis. L162V was not associated with obesity, type 2 diabetes mellitus, hypercholesterolemia, or hypertriglyceridemia.ConclusionsNeither NASH nor genotype 1 HCV-related liver steatosis seems to be associated with the PPARα L162V polymorphism. This polymorphism may have no association with the presence of type 2 diabetes mellitus, obesity, or various blood lipid alterations in NASH and HCV-infected patients. |
doi_str_mv | 10.2310/6650.2005.53706 |
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A recently discovered L162V polymorphism of the PPARα gene is associated with enhanced transcriptional activity. In this study, the frequency of L162V was investigated in nonalcoholic steatohepatitis (NASH) and genotype 1 hepatitis C virus (HCV)-related liver steatosis.MethodsSeventy-two NASH and 141 HCV-infected patients (54 with steatosis, 87 without steatosis) and 119 healthy controls were included. L162V polymorphism of the PPARα gene was analyzed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP).ResultsPCR and RFLP analysis of the related gene segment was successful in 93%, 96%, and 100% of NASH and HCV-infected patients and controls, respectively. The frequency of the L162V polymorphism was similar in the NASH and HCV-infected patients and controls (5.9%, 3.6%, and 2.5%, respectively). No difference in the frequency of this polymorphism was observed in HCV-infected patients with or without significant liver steatosis. L162V was not associated with obesity, type 2 diabetes mellitus, hypercholesterolemia, or hypertriglyceridemia.ConclusionsNeither NASH nor genotype 1 HCV-related liver steatosis seems to be associated with the PPARα L162V polymorphism. This polymorphism may have no association with the presence of type 2 diabetes mellitus, obesity, or various blood lipid alterations in NASH and HCV-infected patients.</description><identifier>ISSN: 1081-5589</identifier><identifier>EISSN: 1708-8267</identifier><identifier>DOI: 10.2310/6650.2005.53706</identifier><identifier>PMID: 16297361</identifier><language>eng</language><publisher>Los Angeles, CA: SAGE Publications</publisher><subject>Adult ; Base Sequence ; Body Mass Index ; Case-Control Studies ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - genetics ; DNA - genetics ; Fatty Liver - complications ; Fatty Liver - genetics ; Fatty Liver - pathology ; Female ; Genotype ; Hepacivirus - genetics ; Hepatitis C, Chronic - complications ; Hepatitis C, Chronic - genetics ; Hepatitis C, Chronic - virology ; Humans ; Hyperlipidemias - complications ; Hyperlipidemias - genetics ; Male ; Middle Aged ; Polymorphism, Genetic ; PPAR alpha - genetics</subject><ispartof>Journal of investigative medicine, 2005-11, Vol.53 (7), p.353-359</ispartof><rights>2015 American Federation for Medical Research, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><rights>2005 American Federation for Medical Research</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b367t-5829ed8985a9edbe7e3e7f1ab112576c2e6e680fa338be274532eb3d6b7c6cfd3</citedby><cites>FETCH-LOGICAL-b367t-5829ed8985a9edbe7e3e7f1ab112576c2e6e680fa338be274532eb3d6b7c6cfd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.2310/6650.2005.53706$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.2310/6650.2005.53706$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,780,784,21819,27924,27925,43621,43622</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16297361$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Verdi, Hasibe</creatorcontrib><creatorcontrib>Sare Koytak, Elif</creatorcontrib><creatorcontrib>Önder, Oğuz</creatorcontrib><creatorcontrib>Arslan Ergül, Ayça</creatorcontrib><creatorcontrib>Cinar, Kubilay</creatorcontrib><creatorcontrib>Idilman, Ramazan</creatorcontrib><creatorcontrib>Erden, Esra</creatorcontrib><creatorcontrib>Mithat Bozdayi, Abdurrahman</creatorcontrib><creatorcontrib>Yurdaydin, Cihan</creatorcontrib><creatorcontrib>Uzunalimoglu, Özden</creatorcontrib><creatorcontrib>Bozkaya, Hakan</creatorcontrib><title>Peroxisome Proliferator-Activated Receptor α L162V Polymorphism in Nonalcoholic Steatohepatitis and Genotype 1 Hepatitis C Virus-Related Liver Steatosis</title><title>Journal of investigative medicine</title><addtitle>J Investig Med</addtitle><description>BackgroundPeroxisome proliferator-activated receptor α (PPARα) plays important roles in lipid metabolism. A recently discovered L162V polymorphism of the PPARα gene is associated with enhanced transcriptional activity. In this study, the frequency of L162V was investigated in nonalcoholic steatohepatitis (NASH) and genotype 1 hepatitis C virus (HCV)-related liver steatosis.MethodsSeventy-two NASH and 141 HCV-infected patients (54 with steatosis, 87 without steatosis) and 119 healthy controls were included. L162V polymorphism of the PPARα gene was analyzed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP).ResultsPCR and RFLP analysis of the related gene segment was successful in 93%, 96%, and 100% of NASH and HCV-infected patients and controls, respectively. The frequency of the L162V polymorphism was similar in the NASH and HCV-infected patients and controls (5.9%, 3.6%, and 2.5%, respectively). No difference in the frequency of this polymorphism was observed in HCV-infected patients with or without significant liver steatosis. L162V was not associated with obesity, type 2 diabetes mellitus, hypercholesterolemia, or hypertriglyceridemia.ConclusionsNeither NASH nor genotype 1 HCV-related liver steatosis seems to be associated with the PPARα L162V polymorphism. This polymorphism may have no association with the presence of type 2 diabetes mellitus, obesity, or various blood lipid alterations in NASH and HCV-infected patients.</description><subject>Adult</subject><subject>Base Sequence</subject><subject>Body Mass Index</subject><subject>Case-Control Studies</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>DNA - genetics</subject><subject>Fatty Liver - complications</subject><subject>Fatty Liver - genetics</subject><subject>Fatty Liver - pathology</subject><subject>Female</subject><subject>Genotype</subject><subject>Hepacivirus - genetics</subject><subject>Hepatitis C, Chronic - complications</subject><subject>Hepatitis C, Chronic - genetics</subject><subject>Hepatitis C, Chronic - virology</subject><subject>Humans</subject><subject>Hyperlipidemias - complications</subject><subject>Hyperlipidemias - genetics</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Polymorphism, Genetic</subject><subject>PPAR alpha - genetics</subject><issn>1081-5589</issn><issn>1708-8267</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1uFDEQhS0EIiGwZoe8YoHoxD_jn15Go5AgjWAUIFvL7a5mPOpuN7Y7Yo7CMbgIZ8KTGcEOVlWq-t4rqR5CLyk5Z5ySCylF6QgR54IrIh-hU6qIrjST6nHpiaaVELo-Qc9S2hLCpKjZU3RCJasVl_QU_VhDDN99CgPgdQy97yDaHGJ16bK_txlafAsOpjLCv37iVVHe4XXod0OI08anAfsRfwij7V3YFLnDnzIUgw1MNvvsE7Zji69hDHk3Aab45s9iie98nFN1C_3DnZW_h3iUJ5-eoyed7RO8ONYz9OXd1eflTbX6eP1-ebmqGi5VroRmNbS61sKW2oACDqqjtqGUCSUdAwlSk85yrhtgaiE4g4a3slFOuq7lZ-j1wXeK4dsMKZvBJwd9b0cIczJSayoWelHAiwPoYkgpQmem6Acbd4YSs0_D7NMw-zTMQxpF8epoPTcDtH_54_sL8PYAJPsVzDbMsTwy_cPvzQFvhu1_j_8GE-Gh-A</recordid><startdate>20051101</startdate><enddate>20051101</enddate><creator>Verdi, Hasibe</creator><creator>Sare Koytak, Elif</creator><creator>Önder, Oğuz</creator><creator>Arslan Ergül, Ayça</creator><creator>Cinar, Kubilay</creator><creator>Idilman, Ramazan</creator><creator>Erden, Esra</creator><creator>Mithat Bozdayi, Abdurrahman</creator><creator>Yurdaydin, Cihan</creator><creator>Uzunalimoglu, Özden</creator><creator>Bozkaya, Hakan</creator><general>SAGE Publications</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>7X8</scope></search><sort><creationdate>20051101</creationdate><title>Peroxisome Proliferator-Activated Receptor α L162V Polymorphism in Nonalcoholic Steatohepatitis and Genotype 1 Hepatitis C Virus-Related Liver Steatosis</title><author>Verdi, Hasibe ; Sare Koytak, Elif ; Önder, Oğuz ; Arslan Ergül, Ayça ; Cinar, Kubilay ; Idilman, Ramazan ; Erden, Esra ; Mithat Bozdayi, Abdurrahman ; Yurdaydin, Cihan ; Uzunalimoglu, Özden ; Bozkaya, Hakan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b367t-5829ed8985a9edbe7e3e7f1ab112576c2e6e680fa338be274532eb3d6b7c6cfd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adult</topic><topic>Base Sequence</topic><topic>Body Mass Index</topic><topic>Case-Control Studies</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>DNA - genetics</topic><topic>Fatty Liver - complications</topic><topic>Fatty Liver - genetics</topic><topic>Fatty Liver - pathology</topic><topic>Female</topic><topic>Genotype</topic><topic>Hepacivirus - genetics</topic><topic>Hepatitis C, Chronic - complications</topic><topic>Hepatitis C, Chronic - genetics</topic><topic>Hepatitis C, Chronic - virology</topic><topic>Humans</topic><topic>Hyperlipidemias - complications</topic><topic>Hyperlipidemias - genetics</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Polymorphism, Genetic</topic><topic>PPAR alpha - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Verdi, Hasibe</creatorcontrib><creatorcontrib>Sare Koytak, Elif</creatorcontrib><creatorcontrib>Önder, Oğuz</creatorcontrib><creatorcontrib>Arslan Ergül, Ayça</creatorcontrib><creatorcontrib>Cinar, Kubilay</creatorcontrib><creatorcontrib>Idilman, Ramazan</creatorcontrib><creatorcontrib>Erden, Esra</creatorcontrib><creatorcontrib>Mithat Bozdayi, Abdurrahman</creatorcontrib><creatorcontrib>Yurdaydin, Cihan</creatorcontrib><creatorcontrib>Uzunalimoglu, Özden</creatorcontrib><creatorcontrib>Bozkaya, Hakan</creatorcontrib><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>Journal of investigative medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Verdi, Hasibe</au><au>Sare Koytak, Elif</au><au>Önder, Oğuz</au><au>Arslan Ergül, Ayça</au><au>Cinar, Kubilay</au><au>Idilman, Ramazan</au><au>Erden, Esra</au><au>Mithat Bozdayi, Abdurrahman</au><au>Yurdaydin, Cihan</au><au>Uzunalimoglu, Özden</au><au>Bozkaya, Hakan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Peroxisome Proliferator-Activated Receptor α L162V Polymorphism in Nonalcoholic Steatohepatitis and Genotype 1 Hepatitis C Virus-Related Liver Steatosis</atitle><jtitle>Journal of investigative medicine</jtitle><addtitle>J Investig Med</addtitle><date>2005-11-01</date><risdate>2005</risdate><volume>53</volume><issue>7</issue><spage>353</spage><epage>359</epage><pages>353-359</pages><issn>1081-5589</issn><eissn>1708-8267</eissn><abstract>BackgroundPeroxisome proliferator-activated receptor α (PPARα) plays important roles in lipid metabolism. A recently discovered L162V polymorphism of the PPARα gene is associated with enhanced transcriptional activity. In this study, the frequency of L162V was investigated in nonalcoholic steatohepatitis (NASH) and genotype 1 hepatitis C virus (HCV)-related liver steatosis.MethodsSeventy-two NASH and 141 HCV-infected patients (54 with steatosis, 87 without steatosis) and 119 healthy controls were included. L162V polymorphism of the PPARα gene was analyzed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP).ResultsPCR and RFLP analysis of the related gene segment was successful in 93%, 96%, and 100% of NASH and HCV-infected patients and controls, respectively. The frequency of the L162V polymorphism was similar in the NASH and HCV-infected patients and controls (5.9%, 3.6%, and 2.5%, respectively). No difference in the frequency of this polymorphism was observed in HCV-infected patients with or without significant liver steatosis. L162V was not associated with obesity, type 2 diabetes mellitus, hypercholesterolemia, or hypertriglyceridemia.ConclusionsNeither NASH nor genotype 1 HCV-related liver steatosis seems to be associated with the PPARα L162V polymorphism. This polymorphism may have no association with the presence of type 2 diabetes mellitus, obesity, or various blood lipid alterations in NASH and HCV-infected patients.</abstract><cop>Los Angeles, CA</cop><pub>SAGE Publications</pub><pmid>16297361</pmid><doi>10.2310/6650.2005.53706</doi><tpages>7</tpages></addata></record> |
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subjects | Adult Base Sequence Body Mass Index Case-Control Studies Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - genetics DNA - genetics Fatty Liver - complications Fatty Liver - genetics Fatty Liver - pathology Female Genotype Hepacivirus - genetics Hepatitis C, Chronic - complications Hepatitis C, Chronic - genetics Hepatitis C, Chronic - virology Humans Hyperlipidemias - complications Hyperlipidemias - genetics Male Middle Aged Polymorphism, Genetic PPAR alpha - genetics |
title | Peroxisome Proliferator-Activated Receptor α L162V Polymorphism in Nonalcoholic Steatohepatitis and Genotype 1 Hepatitis C Virus-Related Liver Steatosis |
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