Source:http://linkedlifedata.com/resource/pubmed/id/16936218
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
9
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| pubmed:dateCreated |
2006-8-28
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| pubmed:abstractText |
Transcription factor 7-like 2 (TCF7L2) regulates genes involved in cell proliferation and differentiation. The TCF7L2 gene is located on chromosome 10q25 in a region of replicated linkage to type 2 diabetes. Recently, a microsatellite marker in intron 3 (DG10S478) and five correlated single nucleotide polymorphisms (SNPs) were identified in Icelandic individuals that showed strong association with type 2 diabetes, which was replicated in Danish and European-American cohorts. We genotyped four of the SNPs (rs7901695, rs7903146, rs11196205, and rs12255372) in Amish subjects with type 2 diabetes (n = 137), impaired glucose tolerance (IGT; n = 139), and normal glucose tolerance (NGT; n = 342). We compared genotype frequencies in subjects with type 2 diabetes with those with NGT and found marginal association for rs7901695 (P = 0.05; odds ratio [OR] 1.51); comparison between NGT control subjects and the combined type 2 diabetes/IGT case group showed strong association with rs7901695 and rs7903146 (P = 0.008-0.01; OR 1.53-1.57) and marginal association with rs11196205 and rs12255372 (P = 0.07 and P = 0.04, respectively). In an expanded set of 698 Amish subjects without diabetes, we found no association with insulin and glucose levels during a 3-h oral glucose tolerance test. We also genotyped these SNPs in nondiabetic, non-Amish subjects (n = 48), in whom intravenous glucose tolerance tests were performed, and found an association between rs7901695 and rs7903146 and insulin sensitivity (P = 0.003 and P = 0.005, respectively) and disposition index (P = 0.04 and P = 0.007, respectively). These data provide replicating evidence that variants in TCF7L2 increase the risk for type 2 diabetes and novel evidence that the variants likely influence both insulin secretion and insulin sensitivity.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/TCF Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/TCF7L2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor 7-Like 2...
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| pubmed:status |
MEDLINE
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| pubmed:month |
Sep
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| pubmed:issn |
0012-1797
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
55
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2654-9
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| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:16936218-Adult,
pubmed-meshheading:16936218-Aged,
pubmed-meshheading:16936218-Blood Glucose,
pubmed-meshheading:16936218-Diabetes Mellitus, Type 2,
pubmed-meshheading:16936218-Ethnic Groups,
pubmed-meshheading:16936218-European Continental Ancestry Group,
pubmed-meshheading:16936218-Female,
pubmed-meshheading:16936218-Gene Frequency,
pubmed-meshheading:16936218-Humans,
pubmed-meshheading:16936218-Insulin,
pubmed-meshheading:16936218-Insulin Resistance,
pubmed-meshheading:16936218-Linkage Disequilibrium,
pubmed-meshheading:16936218-Male,
pubmed-meshheading:16936218-Middle Aged,
pubmed-meshheading:16936218-Pennsylvania,
pubmed-meshheading:16936218-Polymorphism, Single Nucleotide,
pubmed-meshheading:16936218-TCF Transcription Factors,
pubmed-meshheading:16936218-Transcription Factor 7-Like 2 Protein
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| pubmed:year |
2006
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| pubmed:articleTitle |
Polymorphisms in the transcription factor 7-like 2 (TCF7L2) gene are associated with type 2 diabetes in the Amish: replication and evidence for a role in both insulin secretion and insulin resistance.
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| pubmed:affiliation |
Division of Endocrinology, Diabetes and Nutrition, University of Maryland School of Medicine, Baltimore, MD 21201, USA. cdamcott@medicine.umaryland.edu
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, N.I.H., Extramural
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