TCF7L2 Polymorphisms and Progression to Diabetes in the Diabetes Prevention Program
This study examined two polymorphisms of the transcription factor 7–like 2 gene ( TCF7L2 ) to predict the progression to diabetes among subjects with impaired glucose tolerance who were enrolled in the Diabetes Prevention Program, in which lifestyle intervention and treatment with metformin were eac...
Gespeichert in:
| Veröffentlicht in: | The New England journal of medicine 2006-07, Vol.355 (3), p.241-250 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 250 |
|---|---|
| container_issue | 3 |
| container_start_page | 241 |
| container_title | The New England journal of medicine |
| container_volume | 355 |
| creator | Florez, Jose C Jablonski, Kathleen A Bayley, Nick Pollin, Toni I de Bakker, Paul I.W Shuldiner, Alan R Knowler, William C Nathan, David M Altshuler, David |
| description | This study examined two polymorphisms of the transcription factor 7–like 2 gene (
TCF7L2
) to predict the progression to diabetes among subjects with impaired glucose tolerance who were enrolled in the Diabetes Prevention Program, in which lifestyle intervention and treatment with metformin were each compared with placebo. Results indicate that common variants in
TCF7L2
seem to be associated with an increased risk of the development of diabetes among persons with impaired glucose tolerance.
Common variants in the transcription factor 7–like 2 gene (
TCF7L2
) seem to be associated with an increased risk of diabetes among persons with impaired glucose tolerance.
The risk of type 2 diabetes is strongly influenced by inheritance.
1
Genetic susceptibility to the common form of type 2 diabetes appears polygenic — that is, it involves a number of variants, each with a modest effect on the risk of disease in an individual person.
2
Despite important advances in understanding the genetic determinants of the relatively rare monogenic forms of diabetes,
3
the pace of definitive identification of genes that increase the risk of common type 2 diabetes has been slow.
Recently, Grant and colleagues
4
reported on the association of a common microsatellite (DG10S478) within intron 3 of the transcription . . . |
| doi_str_mv | 10.1056/NEJMoa062418 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1762036</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1081574201</sourcerecordid><originalsourceid>FETCH-LOGICAL-c548t-2d98d278ece9bb504f05ea40420cb4edf4458e3dde6a48e7b930b7f87afe196d3</originalsourceid><addsrcrecordid>eNqF0UtvEzEQAGALgWgo3DijFQJOLPj9uCChtOWhAJEoZ8u7O9s4Wq-DvanUf1-HRKQgJHyxRv48Hs8g9JTgNwQL-fbr-ecv0WFJOdH30IwIxmrOsbyPZhhTXXNl2Al6lPMal0W4eYhOiNRCUMln6Pvl_EItaLWMw02IabPyOeTKjV21TPEqQc4-jtUUqzPvGpggV76EKzjGywTXME479uuKC4_Rg94NGZ4c9lP04-L8cv6xXnz78Gn-flG3guuppp3RHVUaWjBNIzDvsQDHMae4bTh0PedCA-s6kI5rUI1huFG9Vq4HYmTHTtG7fd7NtgnQtaWK5Aa7ST64dGOj8_bPk9Gv7FW8tkRJipksCV4dEqT4cwt5ssHnFobBjRC32UotJRalf_-DxAi963-Bz_-C67hNY-mCpZQZRpViBb3eozbFnBP0v0sm2O5mau_OtPBnd795xIchFvDyAFxu3dAnN7Y-H50yEiuDi3uxdyFkO8I6_Pu9W38TtVI</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>223932773</pqid></control><display><type>article</type><title>TCF7L2 Polymorphisms and Progression to Diabetes in the Diabetes Prevention Program</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>New England Journal of Medicine</source><creator>Florez, Jose C ; Jablonski, Kathleen A ; Bayley, Nick ; Pollin, Toni I ; de Bakker, Paul I.W ; Shuldiner, Alan R ; Knowler, William C ; Nathan, David M ; Altshuler, David</creator><creatorcontrib>Florez, Jose C ; Jablonski, Kathleen A ; Bayley, Nick ; Pollin, Toni I ; de Bakker, Paul I.W ; Shuldiner, Alan R ; Knowler, William C ; Nathan, David M ; Altshuler, David ; Diabetes Prevention Program Research Group</creatorcontrib><description>This study examined two polymorphisms of the transcription factor 7–like 2 gene (
TCF7L2
) to predict the progression to diabetes among subjects with impaired glucose tolerance who were enrolled in the Diabetes Prevention Program, in which lifestyle intervention and treatment with metformin were each compared with placebo. Results indicate that common variants in
TCF7L2
seem to be associated with an increased risk of the development of diabetes among persons with impaired glucose tolerance.
Common variants in the transcription factor 7–like 2 gene (
TCF7L2
) seem to be associated with an increased risk of diabetes among persons with impaired glucose tolerance.
The risk of type 2 diabetes is strongly influenced by inheritance.
1
Genetic susceptibility to the common form of type 2 diabetes appears polygenic — that is, it involves a number of variants, each with a modest effect on the risk of disease in an individual person.
2
Despite important advances in understanding the genetic determinants of the relatively rare monogenic forms of diabetes,
3
the pace of definitive identification of genes that increase the risk of common type 2 diabetes has been slow.
Recently, Grant and colleagues
4
reported on the association of a common microsatellite (DG10S478) within intron 3 of the transcription . . .</description><identifier>ISSN: 0028-4793</identifier><identifier>EISSN: 1533-4406</identifier><identifier>DOI: 10.1056/NEJMoa062418</identifier><identifier>PMID: 16855264</identifier><identifier>CODEN: NEJMAG</identifier><language>eng</language><publisher>Boston, MA: Massachusetts Medical Society</publisher><subject>Biological and medical sciences ; Cohort Studies ; Confidence intervals ; Diabetes ; Diabetes Mellitus, Type 2 - epidemiology ; Diabetes Mellitus, Type 2 - genetics ; Diabetes. Impaired glucose tolerance ; Disease Progression ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Enteroendocrine Cells - pathology ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Gene Frequency ; General aspects ; Genetics ; Genotype ; Glucose Metabolism Disorders - genetics ; Humans ; Incidence ; Insulin - metabolism ; Insulin Resistance - genetics ; Insulin Secretion ; Lifestyles ; Linkage Disequilibrium ; Male ; Medical sciences ; Middle Aged ; Polymorphism, Single Nucleotide ; Prevention programs ; Proportional Hazards Models ; Randomized Controlled Trials as Topic ; TCF Transcription Factors - genetics ; Transcription Factor 7-Like 2 Protein</subject><ispartof>The New England journal of medicine, 2006-07, Vol.355 (3), p.241-250</ispartof><rights>Copyright © 2006 Massachusetts Medical Society. All rights reserved.</rights><rights>2006 INIST-CNRS</rights><rights>Copyright 2006 Massachusetts Medical Society.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c548t-2d98d278ece9bb504f05ea40420cb4edf4458e3dde6a48e7b930b7f87afe196d3</citedby><cites>FETCH-LOGICAL-c548t-2d98d278ece9bb504f05ea40420cb4edf4458e3dde6a48e7b930b7f87afe196d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.nejm.org/doi/pdf/10.1056/NEJMoa062418$$EPDF$$P50$$Gmms$$H</linktopdf><linktohtml>$$Uhttps://www.nejm.org/doi/full/10.1056/NEJMoa062418$$EHTML$$P50$$Gmms$$H</linktohtml><link.rule.ids>230,314,776,780,881,2746,2747,26080,27901,27902,52357,54039</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17960790$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16855264$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Florez, Jose C</creatorcontrib><creatorcontrib>Jablonski, Kathleen A</creatorcontrib><creatorcontrib>Bayley, Nick</creatorcontrib><creatorcontrib>Pollin, Toni I</creatorcontrib><creatorcontrib>de Bakker, Paul I.W</creatorcontrib><creatorcontrib>Shuldiner, Alan R</creatorcontrib><creatorcontrib>Knowler, William C</creatorcontrib><creatorcontrib>Nathan, David M</creatorcontrib><creatorcontrib>Altshuler, David</creatorcontrib><creatorcontrib>Diabetes Prevention Program Research Group</creatorcontrib><title>TCF7L2 Polymorphisms and Progression to Diabetes in the Diabetes Prevention Program</title><title>The New England journal of medicine</title><addtitle>N Engl J Med</addtitle><description>This study examined two polymorphisms of the transcription factor 7–like 2 gene (
TCF7L2
) to predict the progression to diabetes among subjects with impaired glucose tolerance who were enrolled in the Diabetes Prevention Program, in which lifestyle intervention and treatment with metformin were each compared with placebo. Results indicate that common variants in
TCF7L2
seem to be associated with an increased risk of the development of diabetes among persons with impaired glucose tolerance.
Common variants in the transcription factor 7–like 2 gene (
TCF7L2
) seem to be associated with an increased risk of diabetes among persons with impaired glucose tolerance.
The risk of type 2 diabetes is strongly influenced by inheritance.
1
Genetic susceptibility to the common form of type 2 diabetes appears polygenic — that is, it involves a number of variants, each with a modest effect on the risk of disease in an individual person.
2
Despite important advances in understanding the genetic determinants of the relatively rare monogenic forms of diabetes,
3
the pace of definitive identification of genes that increase the risk of common type 2 diabetes has been slow.
Recently, Grant and colleagues
4
reported on the association of a common microsatellite (DG10S478) within intron 3 of the transcription . . .</description><subject>Biological and medical sciences</subject><subject>Cohort Studies</subject><subject>Confidence intervals</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 2 - epidemiology</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Disease Progression</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Enteroendocrine Cells - pathology</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>General aspects</subject><subject>Genetics</subject><subject>Genotype</subject><subject>Glucose Metabolism Disorders - genetics</subject><subject>Humans</subject><subject>Incidence</subject><subject>Insulin - metabolism</subject><subject>Insulin Resistance - genetics</subject><subject>Insulin Secretion</subject><subject>Lifestyles</subject><subject>Linkage Disequilibrium</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Prevention programs</subject><subject>Proportional Hazards Models</subject><subject>Randomized Controlled Trials as Topic</subject><subject>TCF Transcription Factors - genetics</subject><subject>Transcription Factor 7-Like 2 Protein</subject><issn>0028-4793</issn><issn>1533-4406</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqF0UtvEzEQAGALgWgo3DijFQJOLPj9uCChtOWhAJEoZ8u7O9s4Wq-DvanUf1-HRKQgJHyxRv48Hs8g9JTgNwQL-fbr-ecv0WFJOdH30IwIxmrOsbyPZhhTXXNl2Al6lPMal0W4eYhOiNRCUMln6Pvl_EItaLWMw02IabPyOeTKjV21TPEqQc4-jtUUqzPvGpggV76EKzjGywTXME479uuKC4_Rg94NGZ4c9lP04-L8cv6xXnz78Gn-flG3guuppp3RHVUaWjBNIzDvsQDHMae4bTh0PedCA-s6kI5rUI1huFG9Vq4HYmTHTtG7fd7NtgnQtaWK5Aa7ST64dGOj8_bPk9Gv7FW8tkRJipksCV4dEqT4cwt5ssHnFobBjRC32UotJRalf_-DxAi963-Bz_-C67hNY-mCpZQZRpViBb3eozbFnBP0v0sm2O5mau_OtPBnd795xIchFvDyAFxu3dAnN7Y-H50yEiuDi3uxdyFkO8I6_Pu9W38TtVI</recordid><startdate>20060720</startdate><enddate>20060720</enddate><creator>Florez, Jose C</creator><creator>Jablonski, Kathleen A</creator><creator>Bayley, Nick</creator><creator>Pollin, Toni I</creator><creator>de Bakker, Paul I.W</creator><creator>Shuldiner, Alan R</creator><creator>Knowler, William C</creator><creator>Nathan, David M</creator><creator>Altshuler, David</creator><general>Massachusetts Medical Society</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>0TZ</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K0Y</scope><scope>LK8</scope><scope>M0R</scope><scope>M0T</scope><scope>M1P</scope><scope>M2M</scope><scope>M2O</scope><scope>M2P</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20060720</creationdate><title>TCF7L2 Polymorphisms and Progression to Diabetes in the Diabetes Prevention Program</title><author>Florez, Jose C ; Jablonski, Kathleen A ; Bayley, Nick ; Pollin, Toni I ; de Bakker, Paul I.W ; Shuldiner, Alan R ; Knowler, William C ; Nathan, David M ; Altshuler, David</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c548t-2d98d278ece9bb504f05ea40420cb4edf4458e3dde6a48e7b930b7f87afe196d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Biological and medical sciences</topic><topic>Cohort Studies</topic><topic>Confidence intervals</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 2 - epidemiology</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Disease Progression</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Enteroendocrine Cells - pathology</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>General aspects</topic><topic>Genetics</topic><topic>Genotype</topic><topic>Glucose Metabolism Disorders - genetics</topic><topic>Humans</topic><topic>Incidence</topic><topic>Insulin - metabolism</topic><topic>Insulin Resistance - genetics</topic><topic>Insulin Secretion</topic><topic>Lifestyles</topic><topic>Linkage Disequilibrium</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Prevention programs</topic><topic>Proportional Hazards Models</topic><topic>Randomized Controlled Trials as Topic</topic><topic>TCF Transcription Factors - genetics</topic><topic>Transcription Factor 7-Like 2 Protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Florez, Jose C</creatorcontrib><creatorcontrib>Jablonski, Kathleen A</creatorcontrib><creatorcontrib>Bayley, Nick</creatorcontrib><creatorcontrib>Pollin, Toni I</creatorcontrib><creatorcontrib>de Bakker, Paul I.W</creatorcontrib><creatorcontrib>Shuldiner, Alan R</creatorcontrib><creatorcontrib>Knowler, William C</creatorcontrib><creatorcontrib>Nathan, David M</creatorcontrib><creatorcontrib>Altshuler, David</creatorcontrib><creatorcontrib>Diabetes Prevention Program Research Group</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>Pharma and Biotech Premium PRO</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</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>eLibrary</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>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>New England Journal of Medicine</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Healthcare Administration Database</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</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>ProQuest One Psychology</collection><collection>ProQuest Central Basic</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>PubMed Central (Full Participant titles)</collection><jtitle>The New England journal of medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Florez, Jose C</au><au>Jablonski, Kathleen A</au><au>Bayley, Nick</au><au>Pollin, Toni I</au><au>de Bakker, Paul I.W</au><au>Shuldiner, Alan R</au><au>Knowler, William C</au><au>Nathan, David M</au><au>Altshuler, David</au><aucorp>Diabetes Prevention Program Research Group</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TCF7L2 Polymorphisms and Progression to Diabetes in the Diabetes Prevention Program</atitle><jtitle>The New England journal of medicine</jtitle><addtitle>N Engl J Med</addtitle><date>2006-07-20</date><risdate>2006</risdate><volume>355</volume><issue>3</issue><spage>241</spage><epage>250</epage><pages>241-250</pages><issn>0028-4793</issn><eissn>1533-4406</eissn><coden>NEJMAG</coden><abstract>This study examined two polymorphisms of the transcription factor 7–like 2 gene (
TCF7L2
) to predict the progression to diabetes among subjects with impaired glucose tolerance who were enrolled in the Diabetes Prevention Program, in which lifestyle intervention and treatment with metformin were each compared with placebo. Results indicate that common variants in
TCF7L2
seem to be associated with an increased risk of the development of diabetes among persons with impaired glucose tolerance.
Common variants in the transcription factor 7–like 2 gene (
TCF7L2
) seem to be associated with an increased risk of diabetes among persons with impaired glucose tolerance.
The risk of type 2 diabetes is strongly influenced by inheritance.
1
Genetic susceptibility to the common form of type 2 diabetes appears polygenic — that is, it involves a number of variants, each with a modest effect on the risk of disease in an individual person.
2
Despite important advances in understanding the genetic determinants of the relatively rare monogenic forms of diabetes,
3
the pace of definitive identification of genes that increase the risk of common type 2 diabetes has been slow.
Recently, Grant and colleagues
4
reported on the association of a common microsatellite (DG10S478) within intron 3 of the transcription . . .</abstract><cop>Boston, MA</cop><pub>Massachusetts Medical Society</pub><pmid>16855264</pmid><doi>10.1056/NEJMoa062418</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0028-4793 |
| ispartof | The New England journal of medicine, 2006-07, Vol.355 (3), p.241-250 |
| issn | 0028-4793 1533-4406 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1762036 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; New England Journal of Medicine |
| subjects | Biological and medical sciences Cohort Studies Confidence intervals Diabetes Diabetes Mellitus, Type 2 - epidemiology Diabetes Mellitus, Type 2 - genetics Diabetes. Impaired glucose tolerance Disease Progression Endocrine pancreas. Apud cells (diseases) Endocrinopathies Enteroendocrine Cells - pathology Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Gene Frequency General aspects Genetics Genotype Glucose Metabolism Disorders - genetics Humans Incidence Insulin - metabolism Insulin Resistance - genetics Insulin Secretion Lifestyles Linkage Disequilibrium Male Medical sciences Middle Aged Polymorphism, Single Nucleotide Prevention programs Proportional Hazards Models Randomized Controlled Trials as Topic TCF Transcription Factors - genetics Transcription Factor 7-Like 2 Protein |
| title | TCF7L2 Polymorphisms and Progression to Diabetes in the Diabetes Prevention Program |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-05T20%3A12%3A20IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=TCF7L2%20Polymorphisms%20and%20Progression%20to%20Diabetes%20in%20the%20Diabetes%20Prevention%20Program&rft.jtitle=The%20New%20England%20journal%20of%20medicine&rft.au=Florez,%20Jose%20C&rft.aucorp=Diabetes%20Prevention%20Program%20Research%20Group&rft.date=2006-07-20&rft.volume=355&rft.issue=3&rft.spage=241&rft.epage=250&rft.pages=241-250&rft.issn=0028-4793&rft.eissn=1533-4406&rft.coden=NEJMAG&rft_id=info:doi/10.1056/NEJMoa062418&rft_dat=%3Cproquest_pubme%3E1081574201%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=223932773&rft_id=info:pmid/16855264&rfr_iscdi=true |