Association of promoter methylation and 32-bp deletion of the PTEN gene with susceptibility to metabolic syndrome
Metabolic syndrome (MeS), a cluster of several metabolic disorders, is increasingly being recognized as a risk factor for type II diabetes (T2D) and cardiovascular disease. Genetic and epigenetic alteration of the phosphatase and tensin homolog deleted on chromosome ten (PTEN) has been associated wi...
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| Veröffentlicht in: | Molecular medicine reports 2013-01, Vol.7 (1), p.342-346 |
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| creator | HASHEMI, MOHAMMAD REZAEI, HAMZEH ESKANDARI-NASAB, EBRAHIM KAYKHAEI, MAHMOUD-ALI TAHERI, MOHSEN |
| description | Metabolic syndrome (MeS), a cluster of several metabolic disorders, is increasingly being recognized as a risk factor for type II diabetes (T2D) and cardiovascular disease. Genetic and epigenetic alteration of the phosphatase and tensin homolog deleted on chromosome ten (PTEN) has been associated with components of MeS. The aim of the present study was to investigate the possible association of a 32-bp deletion polymorphism and promoter methylation of the PTEN gene with MeS. DNA was extracted from the peripheral blood of 151 subjects with and 149 subjects without MeS. The 32-bp deletion variant of PTEN was detected by polymerase chain reaction (PCR) and PTEN promoter methylation was defined by a nested methylation-specific PCR (MSP) method. No significant differences were found in the allelic and genotypic frequencies of the 32-bp deletion variant of PTEN between the groups [odds ratio (OR), 0.77; 95% confidence interval (CI), 0.41-1.45; P=0.431]. However, patients with MeS were identified to have lower levels of PTEN promoter hypermethylation than subjects without MeS. Promoter methylation may be a protective factor against susceptibility to MeS (OR, 0.52; 95% CI, 0.29-0.92; P=0.029). Our findings suggest that PTEN promoter methylation may be a mechanism for PTEN downregulation or silencing in MeS, which remains to be fully clarified. |
| doi_str_mv | 10.3892/mmr.2012.1174 |
| format | Article |
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Genetic and epigenetic alteration of the phosphatase and tensin homolog deleted on chromosome ten (PTEN) has been associated with components of MeS. The aim of the present study was to investigate the possible association of a 32-bp deletion polymorphism and promoter methylation of the PTEN gene with MeS. DNA was extracted from the peripheral blood of 151 subjects with and 149 subjects without MeS. The 32-bp deletion variant of PTEN was detected by polymerase chain reaction (PCR) and PTEN promoter methylation was defined by a nested methylation-specific PCR (MSP) method. No significant differences were found in the allelic and genotypic frequencies of the 32-bp deletion variant of PTEN between the groups [odds ratio (OR), 0.77; 95% confidence interval (CI), 0.41-1.45; P=0.431]. However, patients with MeS were identified to have lower levels of PTEN promoter hypermethylation than subjects without MeS. Promoter methylation may be a protective factor against susceptibility to MeS (OR, 0.52; 95% CI, 0.29-0.92; P=0.029). Our findings suggest that PTEN promoter methylation may be a mechanism for PTEN downregulation or silencing in MeS, which remains to be fully clarified.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2012.1174</identifier><identifier>PMID: 23138198</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Adipocytes ; Adult ; Case-Control Studies ; Cell cycle ; Cholesterol ; Chromosomes ; Confidence intervals ; Deoxyribonucleic acid ; Diabetes ; Diabetes mellitus ; Disease ; DNA ; DNA Methylation ; Female ; Gene deletion ; Gene polymorphism ; Genetic Association Studies ; Genetic Predisposition to Disease ; Humans ; Hypertension ; Insulin resistance ; Kinases ; Male ; Metabolic syndrome ; Metabolic Syndrome - genetics ; Middle Aged ; Mutagenesis, Insertional ; Mutation ; Odds Ratio ; Peripheral blood ; Phosphatase ; Polymerase chain reaction ; polymorphism ; promoter methylation ; Promoter Regions, Genetic ; Proteins ; PTEN ; PTEN Phosphohydrolase - genetics ; PTEN protein ; Rodents ; Sequence Deletion ; Studies ; Tensin</subject><ispartof>Molecular medicine reports, 2013-01, Vol.7 (1), p.342-346</ispartof><rights>Copyright © 2013, Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c392t-122deb60b40b9872206863d42e4bb7c675eca34c5cb25d05a8ceb09a0b29c54d3</citedby><cites>FETCH-LOGICAL-c392t-122deb60b40b9872206863d42e4bb7c675eca34c5cb25d05a8ceb09a0b29c54d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,5555,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23138198$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HASHEMI, MOHAMMAD</creatorcontrib><creatorcontrib>REZAEI, HAMZEH</creatorcontrib><creatorcontrib>ESKANDARI-NASAB, EBRAHIM</creatorcontrib><creatorcontrib>KAYKHAEI, MAHMOUD-ALI</creatorcontrib><creatorcontrib>TAHERI, MOHSEN</creatorcontrib><title>Association of promoter methylation and 32-bp deletion of the PTEN gene with susceptibility to metabolic syndrome</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Metabolic syndrome (MeS), a cluster of several metabolic disorders, is increasingly being recognized as a risk factor for type II diabetes (T2D) and cardiovascular disease. Genetic and epigenetic alteration of the phosphatase and tensin homolog deleted on chromosome ten (PTEN) has been associated with components of MeS. The aim of the present study was to investigate the possible association of a 32-bp deletion polymorphism and promoter methylation of the PTEN gene with MeS. DNA was extracted from the peripheral blood of 151 subjects with and 149 subjects without MeS. The 32-bp deletion variant of PTEN was detected by polymerase chain reaction (PCR) and PTEN promoter methylation was defined by a nested methylation-specific PCR (MSP) method. No significant differences were found in the allelic and genotypic frequencies of the 32-bp deletion variant of PTEN between the groups [odds ratio (OR), 0.77; 95% confidence interval (CI), 0.41-1.45; P=0.431]. However, patients with MeS were identified to have lower levels of PTEN promoter hypermethylation than subjects without MeS. Promoter methylation may be a protective factor against susceptibility to MeS (OR, 0.52; 95% CI, 0.29-0.92; P=0.029). Our findings suggest that PTEN promoter methylation may be a mechanism for PTEN downregulation or silencing in MeS, which remains to be fully clarified.</description><subject>Adipocytes</subject><subject>Adult</subject><subject>Case-Control Studies</subject><subject>Cell cycle</subject><subject>Cholesterol</subject><subject>Chromosomes</subject><subject>Confidence intervals</subject><subject>Deoxyribonucleic acid</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Disease</subject><subject>DNA</subject><subject>DNA Methylation</subject><subject>Female</subject><subject>Gene deletion</subject><subject>Gene polymorphism</subject><subject>Genetic Association Studies</subject><subject>Genetic Predisposition to Disease</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Insulin resistance</subject><subject>Kinases</subject><subject>Male</subject><subject>Metabolic syndrome</subject><subject>Metabolic Syndrome - genetics</subject><subject>Middle Aged</subject><subject>Mutagenesis, Insertional</subject><subject>Mutation</subject><subject>Odds Ratio</subject><subject>Peripheral blood</subject><subject>Phosphatase</subject><subject>Polymerase chain reaction</subject><subject>polymorphism</subject><subject>promoter methylation</subject><subject>Promoter Regions, Genetic</subject><subject>Proteins</subject><subject>PTEN</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN protein</subject><subject>Rodents</subject><subject>Sequence Deletion</subject><subject>Studies</subject><subject>Tensin</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpd0Utv3CAUBWCrapRXs-y2Quqi2TCFCzawjKL0IUVNF-ka8ZoOkW0cgxXNvy_WTLLoCoQ-HV3uaZqPlGyYVPB1GOYNEAobSgV_15xToShmhPD3xzsoJc6ai5yfCOlaaNVpcwaMMkmVPG-eb3JOLpoS04jSFk1zGlIJMxpC2e37w7sZPWKA7YR86MMrLbuAfj_e_UJ_wxjQSyw7lJfswlSijX0se1TSGmNs6qNDeT_6Gh4-NCdb0-dwdTwvmz_f7h5vf-D7h-8_b2_usWMKCqYAPtiOWE6skgKAdLJjnkPg1grXiTY4w7hrnYXWk9ZIFyxRhlhQruWeXTbXh9z6pecl5KKHWKfrezOGtGRNOUghgEpW6ef_6FNa5rFOp6liwFsJalX4oNyccp7DVk9zHMy815TotQtdu9BrF3rtovpPx9TFDsG_6dflV_DlAPJUNxx9ym-mJmEiMKGYMA7sHz48kjM</recordid><startdate>201301</startdate><enddate>201301</enddate><creator>HASHEMI, MOHAMMAD</creator><creator>REZAEI, HAMZEH</creator><creator>ESKANDARI-NASAB, EBRAHIM</creator><creator>KAYKHAEI, MAHMOUD-ALI</creator><creator>TAHERI, MOHSEN</creator><general>D.A. Spandidos</general><general>Spandidos Publications UK Ltd</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>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</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>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>201301</creationdate><title>Association of promoter methylation and 32-bp deletion of the PTEN gene with susceptibility to metabolic syndrome</title><author>HASHEMI, MOHAMMAD ; REZAEI, HAMZEH ; ESKANDARI-NASAB, EBRAHIM ; KAYKHAEI, MAHMOUD-ALI ; TAHERI, MOHSEN</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c392t-122deb60b40b9872206863d42e4bb7c675eca34c5cb25d05a8ceb09a0b29c54d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adipocytes</topic><topic>Adult</topic><topic>Case-Control Studies</topic><topic>Cell cycle</topic><topic>Cholesterol</topic><topic>Chromosomes</topic><topic>Confidence intervals</topic><topic>Deoxyribonucleic acid</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Disease</topic><topic>DNA</topic><topic>DNA Methylation</topic><topic>Female</topic><topic>Gene deletion</topic><topic>Gene polymorphism</topic><topic>Genetic Association Studies</topic><topic>Genetic Predisposition to Disease</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Insulin resistance</topic><topic>Kinases</topic><topic>Male</topic><topic>Metabolic syndrome</topic><topic>Metabolic Syndrome - genetics</topic><topic>Middle Aged</topic><topic>Mutagenesis, Insertional</topic><topic>Mutation</topic><topic>Odds Ratio</topic><topic>Peripheral blood</topic><topic>Phosphatase</topic><topic>Polymerase chain reaction</topic><topic>polymorphism</topic><topic>promoter methylation</topic><topic>Promoter Regions, Genetic</topic><topic>Proteins</topic><topic>PTEN</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN protein</topic><topic>Rodents</topic><topic>Sequence Deletion</topic><topic>Studies</topic><topic>Tensin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HASHEMI, MOHAMMAD</creatorcontrib><creatorcontrib>REZAEI, HAMZEH</creatorcontrib><creatorcontrib>ESKANDARI-NASAB, EBRAHIM</creatorcontrib><creatorcontrib>KAYKHAEI, MAHMOUD-ALI</creatorcontrib><creatorcontrib>TAHERI, MOHSEN</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>Medical Database</collection><collection>Biological Science 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>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HASHEMI, MOHAMMAD</au><au>REZAEI, HAMZEH</au><au>ESKANDARI-NASAB, EBRAHIM</au><au>KAYKHAEI, MAHMOUD-ALI</au><au>TAHERI, MOHSEN</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of promoter methylation and 32-bp deletion of the PTEN gene with susceptibility to metabolic syndrome</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2013-01</date><risdate>2013</risdate><volume>7</volume><issue>1</issue><spage>342</spage><epage>346</epage><pages>342-346</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Metabolic syndrome (MeS), a cluster of several metabolic disorders, is increasingly being recognized as a risk factor for type II diabetes (T2D) and cardiovascular disease. Genetic and epigenetic alteration of the phosphatase and tensin homolog deleted on chromosome ten (PTEN) has been associated with components of MeS. The aim of the present study was to investigate the possible association of a 32-bp deletion polymorphism and promoter methylation of the PTEN gene with MeS. DNA was extracted from the peripheral blood of 151 subjects with and 149 subjects without MeS. The 32-bp deletion variant of PTEN was detected by polymerase chain reaction (PCR) and PTEN promoter methylation was defined by a nested methylation-specific PCR (MSP) method. No significant differences were found in the allelic and genotypic frequencies of the 32-bp deletion variant of PTEN between the groups [odds ratio (OR), 0.77; 95% confidence interval (CI), 0.41-1.45; P=0.431]. However, patients with MeS were identified to have lower levels of PTEN promoter hypermethylation than subjects without MeS. Promoter methylation may be a protective factor against susceptibility to MeS (OR, 0.52; 95% CI, 0.29-0.92; P=0.029). Our findings suggest that PTEN promoter methylation may be a mechanism for PTEN downregulation or silencing in MeS, which remains to be fully clarified.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>23138198</pmid><doi>10.3892/mmr.2012.1174</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Adipocytes Adult Case-Control Studies Cell cycle Cholesterol Chromosomes Confidence intervals Deoxyribonucleic acid Diabetes Diabetes mellitus Disease DNA DNA Methylation Female Gene deletion Gene polymorphism Genetic Association Studies Genetic Predisposition to Disease Humans Hypertension Insulin resistance Kinases Male Metabolic syndrome Metabolic Syndrome - genetics Middle Aged Mutagenesis, Insertional Mutation Odds Ratio Peripheral blood Phosphatase Polymerase chain reaction polymorphism promoter methylation Promoter Regions, Genetic Proteins PTEN PTEN Phosphohydrolase - genetics PTEN protein Rodents Sequence Deletion Studies Tensin |
| title | Association of promoter methylation and 32-bp deletion of the PTEN gene with susceptibility to metabolic syndrome |
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