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Genetic dissection of type 2 diabetes.

Ridderstråle, Martin LU and Groop, Leif LU (2009) In Molecular and Cellular Endocrinology 2008(Oct 19). p.10-17
Abstract
Compared to the successful probing of genetic causes of monogenic disorders, dissecting the genetics of complex polygenic diseases has until recently been a fairly slow and cumbersome process. With the introduction of whole genome wide association studies (WGAS) the situation dramatically changed in 2007. The results from several recent WGAS on type 2 diabetes (T2D) and obesity have identified at least eighteen genes consistently associated with T2D. Many of the genes implicate pancreatic beta-cell function in the pathogenesis of T2D whereas only one clearly associate with insulin resistance. The identified genes most likely merely represent the tip of the iceberg in the explanation behind T2D. Refined tools will have to provide a more... (More)
Compared to the successful probing of genetic causes of monogenic disorders, dissecting the genetics of complex polygenic diseases has until recently been a fairly slow and cumbersome process. With the introduction of whole genome wide association studies (WGAS) the situation dramatically changed in 2007. The results from several recent WGAS on type 2 diabetes (T2D) and obesity have identified at least eighteen genes consistently associated with T2D. Many of the genes implicate pancreatic beta-cell function in the pathogenesis of T2D whereas only one clearly associate with insulin resistance. The identified genes most likely merely represent the tip of the iceberg in the explanation behind T2D. Refined tools will have to provide a more complete picture of the genetic complexity of T2D over the next few years. In addition to common variants increasing susceptibility for the disease, rare variants with stronger effects, copy number variations, and epigenetic effects like DNA methylation and histone acetylation will become important. Nevertheless, today we are able for the first time to anticipate that the genetics of a complex disease like T2D really can be dissected. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Molecular and Cellular Endocrinology
volume
2008
issue
Oct 19
pages
10 - 17
publisher
Elsevier
external identifiers
  • wos:000262600600003
  • pmid:19000735
  • scopus:57649210496
ISSN
1872-8057
DOI
10.1016/j.mce.2008.10.002
language
English
LU publication?
yes
id
b56c0b9b-9a51-42b0-8067-98534f1a2c80 (old id 1271618)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/19000735?dopt=Abstract
date added to LUP
2008-12-03 12:47:51
date last changed
2017-11-05 03:47:29
@article{b56c0b9b-9a51-42b0-8067-98534f1a2c80,
  abstract     = {Compared to the successful probing of genetic causes of monogenic disorders, dissecting the genetics of complex polygenic diseases has until recently been a fairly slow and cumbersome process. With the introduction of whole genome wide association studies (WGAS) the situation dramatically changed in 2007. The results from several recent WGAS on type 2 diabetes (T2D) and obesity have identified at least eighteen genes consistently associated with T2D. Many of the genes implicate pancreatic beta-cell function in the pathogenesis of T2D whereas only one clearly associate with insulin resistance. The identified genes most likely merely represent the tip of the iceberg in the explanation behind T2D. Refined tools will have to provide a more complete picture of the genetic complexity of T2D over the next few years. In addition to common variants increasing susceptibility for the disease, rare variants with stronger effects, copy number variations, and epigenetic effects like DNA methylation and histone acetylation will become important. Nevertheless, today we are able for the first time to anticipate that the genetics of a complex disease like T2D really can be dissected.},
  author       = {Ridderstråle, Martin and Groop, Leif},
  issn         = {1872-8057},
  language     = {eng},
  number       = {Oct 19},
  pages        = {10--17},
  publisher    = {Elsevier},
  series       = {Molecular and Cellular Endocrinology},
  title        = {Genetic dissection of type 2 diabetes.},
  url          = {http://dx.doi.org/10.1016/j.mce.2008.10.002},
  volume       = {2008},
  year         = {2009},
}