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High-density haplotype structure and association testing of the insulin-degrading enzyme (IDE) gene with type 2 diabetes in 4,206 people

Florez, JC; Wiltshire, S; Agapakis, CM; Burtt, NP; de Bakker, PIW; Almgren, Peter LU ; Bostrom, KB; Tuomi, T; Gaudet, D and Daly, MJ, et al. (2006) In Diabetes 55(1). p.128-135
Abstract
The insulin-degrading enzyme is responsible for the intracellular proteolysis of insulin. Its gene IDE is located on chromosome 10, in an area with suggestive linkage to type 2 diabetes and related phenotypes. Due to the impact of genetic variants of this gene in rodents and the function of its protein product, it has been proposed as a candidate gene for type 2 diabetes. Various groups have explored the role of the common genetic variation of IDE on insulin resistance and reported associations of various single nucleotide polymorphisms (SNPs) and haplotypes on both type 2 diabetes and glycemic traits. We sought to characterize the haplotype structure of IDE in detail and replicate the association of common variants with type 2 diabetes,... (More)
The insulin-degrading enzyme is responsible for the intracellular proteolysis of insulin. Its gene IDE is located on chromosome 10, in an area with suggestive linkage to type 2 diabetes and related phenotypes. Due to the impact of genetic variants of this gene in rodents and the function of its protein product, it has been proposed as a candidate gene for type 2 diabetes. Various groups have explored the role of the common genetic variation of IDE on insulin resistance and reported associations of various single nucleotide polymorphisms (SNPs) and haplotypes on both type 2 diabetes and glycemic traits. We sought to characterize the haplotype structure of IDE in detail and replicate the association of common variants with type 2 diabetes, fasting insulin, fasting glucose, and insulin resistance. We assessed linkage disequilibrium, selected single-marker and multimarker tags, and genotyped these markers in several case-control and family-based samples totalling 4,206 Caucasian individuals. We observed no statistically significant evidence of association between single-marker or multimarker tests in IDE and type 2 diabetes. Nominally significant differences in quantitative traits are consistent with statistical noise. We conclude that common genetic variation at, IDE is unlikely to confer clinically significant risk of type 2 diabetes in Caucasians. (Less)
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publishing date
type
Contribution to journal
publication status
published
subject
in
Diabetes
volume
55
issue
1
pages
128 - 135
publisher
American Diabetes Association Inc.
external identifiers
  • wos:000234349500016
  • pmid:16380485
  • scopus:33644772571
ISSN
1939-327X
DOI
10.2337/diabetes.55.01.06.db05-0954
language
English
LU publication?
yes
id
58a75b37-8272-440e-950b-a146508bf61e (old id 421611)
date added to LUP
2007-10-02 20:20:41
date last changed
2019-06-04 02:18:16
@article{58a75b37-8272-440e-950b-a146508bf61e,
  abstract     = {The insulin-degrading enzyme is responsible for the intracellular proteolysis of insulin. Its gene IDE is located on chromosome 10, in an area with suggestive linkage to type 2 diabetes and related phenotypes. Due to the impact of genetic variants of this gene in rodents and the function of its protein product, it has been proposed as a candidate gene for type 2 diabetes. Various groups have explored the role of the common genetic variation of IDE on insulin resistance and reported associations of various single nucleotide polymorphisms (SNPs) and haplotypes on both type 2 diabetes and glycemic traits. We sought to characterize the haplotype structure of IDE in detail and replicate the association of common variants with type 2 diabetes, fasting insulin, fasting glucose, and insulin resistance. We assessed linkage disequilibrium, selected single-marker and multimarker tags, and genotyped these markers in several case-control and family-based samples totalling 4,206 Caucasian individuals. We observed no statistically significant evidence of association between single-marker or multimarker tests in IDE and type 2 diabetes. Nominally significant differences in quantitative traits are consistent with statistical noise. We conclude that common genetic variation at, IDE is unlikely to confer clinically significant risk of type 2 diabetes in Caucasians.},
  author       = {Florez, JC and Wiltshire, S and Agapakis, CM and Burtt, NP and de Bakker, PIW and Almgren, Peter and Bostrom, KB and Tuomi, T and Gaudet, D and Daly, MJ and Hirschhorn, JN and McCarthy, MI and Altshuler, D and Groop, Leif},
  issn         = {1939-327X},
  language     = {eng},
  number       = {1},
  pages        = {128--135},
  publisher    = {American Diabetes Association Inc.},
  series       = {Diabetes},
  title        = {High-density haplotype structure and association testing of the insulin-degrading enzyme (IDE) gene with type 2 diabetes in 4,206 people},
  url          = {http://dx.doi.org/10.2337/diabetes.55.01.06.db05-0954},
  volume       = {55},
  year         = {2006},
}