Dietary saturated fat, gender and genetic variation at the TCF7L2 locus predict the development of metabolic syndrome
Transcription factor 7-like 2 (TCF7L2) is the strongest genetic determinant of type 2 diabetes (T2DM) and insulin-related phenotypes to date. Dietary fat is a key environmental factor which may interact with genotype to affect risk of metabolic syndrome (MetS) and T2DM. This study investigated the r...
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| creator | Phillips, Catherine M Goumidi, Louisa Bertrais, Sandrine Field, Martyn R McManus, Ross Hercberg, Serge Lairon, Denis Planells, Richard Roche, Helen M |
| description | Transcription factor 7-like 2 (TCF7L2) is the strongest genetic determinant of type 2 diabetes (T2DM) and insulin-related phenotypes to date. Dietary fat is a key environmental factor which may interact with genotype to affect risk of metabolic syndrome (MetS) and T2DM. This study investigated the relationship between the TCF7L2 rs7903146 polymorphism, insulin sensitivity/resistance and MetS in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n=1754) and determined potential interactions with dietary fat intake. Female minor T allele carriers of rs7903146 had increased MetS risk (odds ratio [OR] 1.66, confidence interval [CI] 1.02–2.70, P=.04) and displayed elevated insulin concentrations (P=.005), impaired insulin sensitivity (P=.011), increased abdominal obesity (P=.008) and body mass index (P=.001) and higher blood pressure (P |
| doi_str_mv | 10.1016/j.jnutbio.2010.11.020 |
| format | Article |
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Dietary fat is a key environmental factor which may interact with genotype to affect risk of metabolic syndrome (MetS) and T2DM. This study investigated the relationship between the TCF7L2 rs7903146 polymorphism, insulin sensitivity/resistance and MetS in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n=1754) and determined potential interactions with dietary fat intake. Female minor T allele carriers of rs7903146 had increased MetS risk (odds ratio [OR] 1.66, confidence interval [CI] 1.02–2.70, P=.04) and displayed elevated insulin concentrations (P=.005), impaired insulin sensitivity (P=.011), increased abdominal obesity (P=.008) and body mass index (P=.001) and higher blood pressure (P<.05) compared to the CC homozygotes. Metabolic syndrome risk was also modulated by dietary saturated fat (SFA) intake (P=.035 for interaction). High dietary SFA intake (≥15.5% energy) exacerbated MetS risk (OR 2.35, 95% CI 1.29–4.27, P=.005) and was associated with further impaired insulin sensitivity in the T allele carriers relative to the CC homozygotes (P=.025) and particularly to the T allele carriers with the lowest SFA intake (P=.008). No significant genotype effect on MetS risk or insulin sensitivity was evident among low-SFA consumers. In conclusion, the TCF7L2 rs7903146 polymorphism influences MetS risk, which is augmented by both gender and dietary SFA intake, suggesting novel gene–diet–gender interactions.</description><identifier>ISSN: 0955-2863</identifier><identifier>EISSN: 1873-4847</identifier><identifier>DOI: 10.1016/j.jnutbio.2010.11.020</identifier><identifier>PMID: 21543200</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Alleles ; Biological and medical sciences ; Blood pressure ; Body Mass Index ; Case-Control Studies ; confidence interval ; Consumers ; Diabetes mellitus ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - metabolism ; Diet ; dietary fat ; Dietary Fats - metabolism ; DNA - genetics ; DNA - isolation & purification ; Environmental factors ; fat intake ; Fatty Acids - metabolism ; Feeding. Feeding behavior ; Female ; Follow-Up Studies ; Fundamental and applied biological sciences. Psychology ; gender ; Gene polymorphism ; Genetic diversity ; Genetic Loci ; Genetic Predisposition to Disease ; genetic variation ; Gene–diet interaction ; homozygosity ; Homozygote ; Homozygotes ; Humans ; Insulin ; Insulin - blood ; Insulin Resistance ; Insulin sensitivity ; Life Sciences ; LIPGENE ; loci ; Logistic Models ; Male ; Metabolic disorders ; Metabolic syndrome ; Metabolic Syndrome - blood ; Metabolic Syndrome - genetics ; Metabolic Syndrome - metabolism ; Middle Aged ; noninsulin-dependent diabetes mellitus ; Obesity ; odds ratio ; Phenotype ; Polymorphism, Single Nucleotide ; risk ; Risk Factors ; Saturated fat ; Sex Factors ; Surveys and Questionnaires ; TCF7L2 ; Transcription Factor 7-Like 2 Protein - genetics ; Transcription Factor 7-Like 2 Protein - metabolism ; Transcription factors ; Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><ispartof>The Journal of nutritional biochemistry, 2012-03, Vol.23 (3), p.239-244</ispartof><rights>2012 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2012 Elsevier Inc. All rights reserved.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c509t-49a017db457002b71dae97a548ac6109e4f8ee9b4316e75b8c14750fc7730b493</citedby><cites>FETCH-LOGICAL-c509t-49a017db457002b71dae97a548ac6109e4f8ee9b4316e75b8c14750fc7730b493</cites><orcidid>0000-0002-3168-1350 ; 0000-0001-7388-0916</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0955286311000234$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25604713$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21543200$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.inrae.fr/hal-02653080$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Phillips, Catherine M</creatorcontrib><creatorcontrib>Goumidi, Louisa</creatorcontrib><creatorcontrib>Bertrais, Sandrine</creatorcontrib><creatorcontrib>Field, Martyn R</creatorcontrib><creatorcontrib>McManus, Ross</creatorcontrib><creatorcontrib>Hercberg, Serge</creatorcontrib><creatorcontrib>Lairon, Denis</creatorcontrib><creatorcontrib>Planells, Richard</creatorcontrib><creatorcontrib>Roche, Helen M</creatorcontrib><title>Dietary saturated fat, gender and genetic variation at the TCF7L2 locus predict the development of metabolic syndrome</title><title>The Journal of nutritional biochemistry</title><addtitle>J Nutr Biochem</addtitle><description>Transcription factor 7-like 2 (TCF7L2) is the strongest genetic determinant of type 2 diabetes (T2DM) and insulin-related phenotypes to date. Dietary fat is a key environmental factor which may interact with genotype to affect risk of metabolic syndrome (MetS) and T2DM. This study investigated the relationship between the TCF7L2 rs7903146 polymorphism, insulin sensitivity/resistance and MetS in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n=1754) and determined potential interactions with dietary fat intake. Female minor T allele carriers of rs7903146 had increased MetS risk (odds ratio [OR] 1.66, confidence interval [CI] 1.02–2.70, P=.04) and displayed elevated insulin concentrations (P=.005), impaired insulin sensitivity (P=.011), increased abdominal obesity (P=.008) and body mass index (P=.001) and higher blood pressure (P<.05) compared to the CC homozygotes. Metabolic syndrome risk was also modulated by dietary saturated fat (SFA) intake (P=.035 for interaction). High dietary SFA intake (≥15.5% energy) exacerbated MetS risk (OR 2.35, 95% CI 1.29–4.27, P=.005) and was associated with further impaired insulin sensitivity in the T allele carriers relative to the CC homozygotes (P=.025) and particularly to the T allele carriers with the lowest SFA intake (P=.008). No significant genotype effect on MetS risk or insulin sensitivity was evident among low-SFA consumers. In conclusion, the TCF7L2 rs7903146 polymorphism influences MetS risk, which is augmented by both gender and dietary SFA intake, suggesting novel gene–diet–gender interactions.</description><subject>Alleles</subject><subject>Biological and medical sciences</subject><subject>Blood pressure</subject><subject>Body Mass Index</subject><subject>Case-Control Studies</subject><subject>confidence interval</subject><subject>Consumers</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diet</subject><subject>dietary fat</subject><subject>Dietary Fats - metabolism</subject><subject>DNA - genetics</subject><subject>DNA - isolation & purification</subject><subject>Environmental factors</subject><subject>fat intake</subject><subject>Fatty Acids - metabolism</subject><subject>Feeding. Feeding behavior</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>gender</subject><subject>Gene polymorphism</subject><subject>Genetic diversity</subject><subject>Genetic Loci</subject><subject>Genetic Predisposition to Disease</subject><subject>genetic variation</subject><subject>Gene–diet interaction</subject><subject>homozygosity</subject><subject>Homozygote</subject><subject>Homozygotes</subject><subject>Humans</subject><subject>Insulin</subject><subject>Insulin - blood</subject><subject>Insulin Resistance</subject><subject>Insulin sensitivity</subject><subject>Life Sciences</subject><subject>LIPGENE</subject><subject>loci</subject><subject>Logistic Models</subject><subject>Male</subject><subject>Metabolic disorders</subject><subject>Metabolic syndrome</subject><subject>Metabolic Syndrome - blood</subject><subject>Metabolic Syndrome - genetics</subject><subject>Metabolic Syndrome - metabolism</subject><subject>Middle Aged</subject><subject>noninsulin-dependent diabetes mellitus</subject><subject>Obesity</subject><subject>odds ratio</subject><subject>Phenotype</subject><subject>Polymorphism, Single Nucleotide</subject><subject>risk</subject><subject>Risk Factors</subject><subject>Saturated fat</subject><subject>Sex Factors</subject><subject>Surveys and Questionnaires</subject><subject>TCF7L2</subject><subject>Transcription Factor 7-Like 2 Protein - genetics</subject><subject>Transcription Factor 7-Like 2 Protein - metabolism</subject><subject>Transcription factors</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><issn>0955-2863</issn><issn>1873-4847</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFksFu1DAQhi0EotuFRwB8QQWJXcaOHScnVC2UIq3EgfZsOc6k9SqJF9tZqW-PV1nKrZxszXwz_4z-IeQNgzUDVn7erXfjlBrn1xyOMbYGDs_IglWqWIlKqOdkAbWUK16VxRk5j3EHAFzI8iU540yKggMsyPTVYTLhgUaTpmAStrQz6RO9w7HFQM3YHr-YnKUHE5xJzo_UJJrukd5srtSW097bKdJ9wNbZOdHiAXu_H3BM1Hd0yAqN73OL-DC2wQ_4irzoTB_x9eldkturbzeb69X25_cfm8vtykqo00rUBphqGyFVHr1RrDVYKyNFZWzJoEbRVYh1IwpWopJNZZlQEjqrVAGNqIsl-Tj3vTe93gc35E21N05fX271MQa8lAVUcGCZvZjZffC_J4xJDy5a7Hszop-irjkTvFCZX5IPT5IMeAWsYqXIqJxRG3yMAbvHKRjoo496p08-6qOPmrE8E-S6tyeJqRmwfaz6a1wG3p8AE63pu2BG6-I_TpYgFCsy927mOuO1uQuZuf2VlUQ-BgGMyycJzqp8PUvyZSYwW3VwGHS0DkebDQ9ok269-886fwDryc7C</recordid><startdate>20120301</startdate><enddate>20120301</enddate><creator>Phillips, Catherine M</creator><creator>Goumidi, Louisa</creator><creator>Bertrais, Sandrine</creator><creator>Field, Martyn R</creator><creator>McManus, Ross</creator><creator>Hercberg, Serge</creator><creator>Lairon, Denis</creator><creator>Planells, Richard</creator><creator>Roche, Helen M</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>FBQ</scope><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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-3168-1350</orcidid><orcidid>https://orcid.org/0000-0001-7388-0916</orcidid></search><sort><creationdate>20120301</creationdate><title>Dietary saturated fat, gender and genetic variation at the TCF7L2 locus predict the development of metabolic syndrome</title><author>Phillips, Catherine M ; Goumidi, Louisa ; Bertrais, Sandrine ; Field, Martyn R ; McManus, Ross ; Hercberg, Serge ; Lairon, Denis ; Planells, Richard ; Roche, Helen M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c509t-49a017db457002b71dae97a548ac6109e4f8ee9b4316e75b8c14750fc7730b493</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Alleles</topic><topic>Biological and medical sciences</topic><topic>Blood pressure</topic><topic>Body Mass Index</topic><topic>Case-Control Studies</topic><topic>confidence interval</topic><topic>Consumers</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diet</topic><topic>dietary fat</topic><topic>Dietary Fats - metabolism</topic><topic>DNA - genetics</topic><topic>DNA - isolation & purification</topic><topic>Environmental factors</topic><topic>fat intake</topic><topic>Fatty Acids - metabolism</topic><topic>Feeding. Feeding behavior</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>gender</topic><topic>Gene polymorphism</topic><topic>Genetic diversity</topic><topic>Genetic Loci</topic><topic>Genetic Predisposition to Disease</topic><topic>genetic variation</topic><topic>Gene–diet interaction</topic><topic>homozygosity</topic><topic>Homozygote</topic><topic>Homozygotes</topic><topic>Humans</topic><topic>Insulin</topic><topic>Insulin - blood</topic><topic>Insulin Resistance</topic><topic>Insulin sensitivity</topic><topic>Life Sciences</topic><topic>LIPGENE</topic><topic>loci</topic><topic>Logistic Models</topic><topic>Male</topic><topic>Metabolic disorders</topic><topic>Metabolic syndrome</topic><topic>Metabolic Syndrome - blood</topic><topic>Metabolic Syndrome - genetics</topic><topic>Metabolic Syndrome - metabolism</topic><topic>Middle Aged</topic><topic>noninsulin-dependent diabetes mellitus</topic><topic>Obesity</topic><topic>odds ratio</topic><topic>Phenotype</topic><topic>Polymorphism, Single Nucleotide</topic><topic>risk</topic><topic>Risk Factors</topic><topic>Saturated fat</topic><topic>Sex Factors</topic><topic>Surveys and Questionnaires</topic><topic>TCF7L2</topic><topic>Transcription Factor 7-Like 2 Protein - genetics</topic><topic>Transcription Factor 7-Like 2 Protein - metabolism</topic><topic>Transcription factors</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Phillips, Catherine M</creatorcontrib><creatorcontrib>Goumidi, Louisa</creatorcontrib><creatorcontrib>Bertrais, Sandrine</creatorcontrib><creatorcontrib>Field, Martyn R</creatorcontrib><creatorcontrib>McManus, Ross</creatorcontrib><creatorcontrib>Hercberg, Serge</creatorcontrib><creatorcontrib>Lairon, Denis</creatorcontrib><creatorcontrib>Planells, Richard</creatorcontrib><creatorcontrib>Roche, Helen M</creatorcontrib><collection>AGRIS</collection><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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>The Journal of nutritional biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Phillips, Catherine M</au><au>Goumidi, Louisa</au><au>Bertrais, Sandrine</au><au>Field, Martyn R</au><au>McManus, Ross</au><au>Hercberg, Serge</au><au>Lairon, Denis</au><au>Planells, Richard</au><au>Roche, Helen M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dietary saturated fat, gender and genetic variation at the TCF7L2 locus predict the development of metabolic syndrome</atitle><jtitle>The Journal of nutritional biochemistry</jtitle><addtitle>J Nutr Biochem</addtitle><date>2012-03-01</date><risdate>2012</risdate><volume>23</volume><issue>3</issue><spage>239</spage><epage>244</epage><pages>239-244</pages><issn>0955-2863</issn><eissn>1873-4847</eissn><abstract>Transcription factor 7-like 2 (TCF7L2) is the strongest genetic determinant of type 2 diabetes (T2DM) and insulin-related phenotypes to date. Dietary fat is a key environmental factor which may interact with genotype to affect risk of metabolic syndrome (MetS) and T2DM. This study investigated the relationship between the TCF7L2 rs7903146 polymorphism, insulin sensitivity/resistance and MetS in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n=1754) and determined potential interactions with dietary fat intake. Female minor T allele carriers of rs7903146 had increased MetS risk (odds ratio [OR] 1.66, confidence interval [CI] 1.02–2.70, P=.04) and displayed elevated insulin concentrations (P=.005), impaired insulin sensitivity (P=.011), increased abdominal obesity (P=.008) and body mass index (P=.001) and higher blood pressure (P<.05) compared to the CC homozygotes. Metabolic syndrome risk was also modulated by dietary saturated fat (SFA) intake (P=.035 for interaction). High dietary SFA intake (≥15.5% energy) exacerbated MetS risk (OR 2.35, 95% CI 1.29–4.27, P=.005) and was associated with further impaired insulin sensitivity in the T allele carriers relative to the CC homozygotes (P=.025) and particularly to the T allele carriers with the lowest SFA intake (P=.008). No significant genotype effect on MetS risk or insulin sensitivity was evident among low-SFA consumers. In conclusion, the TCF7L2 rs7903146 polymorphism influences MetS risk, which is augmented by both gender and dietary SFA intake, suggesting novel gene–diet–gender interactions.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>21543200</pmid><doi>10.1016/j.jnutbio.2010.11.020</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0002-3168-1350</orcidid><orcidid>https://orcid.org/0000-0001-7388-0916</orcidid></addata></record> |
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| subjects | Alleles Biological and medical sciences Blood pressure Body Mass Index Case-Control Studies confidence interval Consumers Diabetes mellitus Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - metabolism Diet dietary fat Dietary Fats - metabolism DNA - genetics DNA - isolation & purification Environmental factors fat intake Fatty Acids - metabolism Feeding. Feeding behavior Female Follow-Up Studies Fundamental and applied biological sciences. Psychology gender Gene polymorphism Genetic diversity Genetic Loci Genetic Predisposition to Disease genetic variation Gene–diet interaction homozygosity Homozygote Homozygotes Humans Insulin Insulin - blood Insulin Resistance Insulin sensitivity Life Sciences LIPGENE loci Logistic Models Male Metabolic disorders Metabolic syndrome Metabolic Syndrome - blood Metabolic Syndrome - genetics Metabolic Syndrome - metabolism Middle Aged noninsulin-dependent diabetes mellitus Obesity odds ratio Phenotype Polymorphism, Single Nucleotide risk Risk Factors Saturated fat Sex Factors Surveys and Questionnaires TCF7L2 Transcription Factor 7-Like 2 Protein - genetics Transcription Factor 7-Like 2 Protein - metabolism Transcription factors Vertebrates: anatomy and physiology, studies on body, several organs or systems |
| title | Dietary saturated fat, gender and genetic variation at the TCF7L2 locus predict the development of metabolic syndrome |
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