Common single nucleotide polymorphisms in TCF7L2 are reproducibly associated with type 2 diabetes and reduce the insulin response to glucose in nondiabetic individuals
(2006) In Diabetes 55(10). p.2890-2895- Abstract
- Recently, common noncoding variants in the TCF7L2 gene were strongly associated with increased risk of type 2 diabetes in samples from Iceland, Denmark, and the U.S. We genotyped 13 single nucleotide polymorphisms (SNPs) across TCF7L2 in 8,310 individuals in family-based and case-control designs from Scandinavia, Poland, and the U.S. We convincingly confirmed the previous association of TCF7L2 SNPs with the risk of type 2 diabetes (rs7903146T odds ratio 1.40 [95% CI 1.30-1.50], P = 6.74 x 10(-20)). In nondiabetic individuals, the risk genotypes were associated with a substantial reduction in the insulinogenic index derived from an oral glucose tolerance test (risk allele homozygotes have half the insulin response to glucose of noncarriers,... (More)
- Recently, common noncoding variants in the TCF7L2 gene were strongly associated with increased risk of type 2 diabetes in samples from Iceland, Denmark, and the U.S. We genotyped 13 single nucleotide polymorphisms (SNPs) across TCF7L2 in 8,310 individuals in family-based and case-control designs from Scandinavia, Poland, and the U.S. We convincingly confirmed the previous association of TCF7L2 SNPs with the risk of type 2 diabetes (rs7903146T odds ratio 1.40 [95% CI 1.30-1.50], P = 6.74 x 10(-20)). In nondiabetic individuals, the risk genotypes were associated with a substantial reduction in the insulinogenic index derived from an oral glucose tolerance test (risk allele homozygotes have half the insulin response to glucose of noncarriers, P = 0.003) but not with increased insulin resistance. These results suggest that TCF7L2 variants may act through insulin secretion to increase the risk of type 2 diabetes. (Less)
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https://lup.lub.lu.se/record/389625
- author
- organization
- publishing date
- 2006
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Diabetes
- volume
- 55
- issue
- 10
- pages
- 2890 - 2895
- publisher
- American Diabetes Association Inc.
- external identifiers
-
- pmid:17003358
- wos:000240910400029
- scopus:33750892139
- pmid:17003358
- ISSN
- 1939-327X
- DOI
- 10.2337/db06-0381
- language
- English
- LU publication?
- yes
- id
- 66968ad6-6972-4e40-a882-57d0ebf5cd0a (old id 389625)
- date added to LUP
- 2016-04-01 16:35:09
- date last changed
- 2024-05-10 06:42:09
@article{66968ad6-6972-4e40-a882-57d0ebf5cd0a, abstract = {{Recently, common noncoding variants in the TCF7L2 gene were strongly associated with increased risk of type 2 diabetes in samples from Iceland, Denmark, and the U.S. We genotyped 13 single nucleotide polymorphisms (SNPs) across TCF7L2 in 8,310 individuals in family-based and case-control designs from Scandinavia, Poland, and the U.S. We convincingly confirmed the previous association of TCF7L2 SNPs with the risk of type 2 diabetes (rs7903146T odds ratio 1.40 [95% CI 1.30-1.50], P = 6.74 x 10(-20)). In nondiabetic individuals, the risk genotypes were associated with a substantial reduction in the insulinogenic index derived from an oral glucose tolerance test (risk allele homozygotes have half the insulin response to glucose of noncarriers, P = 0.003) but not with increased insulin resistance. These results suggest that TCF7L2 variants may act through insulin secretion to increase the risk of type 2 diabetes.}}, author = {{Saxena, Richa and Gianniny, Lauren and Burtt, Noel P. and Lyssenko, Valeriya and Giuducci, Candace and Sjögren, Marketa and Florez, Jose C. and Almgren, Peter and Isomaa, Bo and Orho-Melander, Marju and Lindblad, Ulf and Daly, Mark J. and Tuomi, Tiinamaija and Hirschhorn, Joel N. and Ardlie, Kristin G. and Groop, Leif and Altshuler, David}}, issn = {{1939-327X}}, language = {{eng}}, number = {{10}}, pages = {{2890--2895}}, publisher = {{American Diabetes Association Inc.}}, series = {{Diabetes}}, title = {{Common single nucleotide polymorphisms in TCF7L2 are reproducibly associated with type 2 diabetes and reduce the insulin response to glucose in nondiabetic individuals}}, url = {{http://dx.doi.org/10.2337/db06-0381}}, doi = {{10.2337/db06-0381}}, volume = {{55}}, year = {{2006}}, }