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Genetic basis of beta-cell dysfunction in man.

Groop, Leif LU and Lyssenko, Valeriya LU (2009) In Diabetes, Obesity and Metabolism 11 Suppl 4. p.149-158
Abstract
Although the genetic causes of monogenic disorders have been successfully identified in the past, the success in dissecting the genetics of complex polygenic diseases has until now been limited. With the introduction of whole genome wide association studies (WGAS) in 2007, the picture has been dramatically changed. Today we know of about 20 genetic variants increasing the risk of type 2 diabetes (T2D). Most of them seem to influence the capacity of beta-cells to increase insulin secretion to meet the demands imposed by an increase in body weight and insulin resistance. This probably represents only the tip of the iceberg, and over the next few years refined tools will provide a more complete picture of the genetic complexity of T2D. This... (More)
Although the genetic causes of monogenic disorders have been successfully identified in the past, the success in dissecting the genetics of complex polygenic diseases has until now been limited. With the introduction of whole genome wide association studies (WGAS) in 2007, the picture has been dramatically changed. Today we know of about 20 genetic variants increasing the risk of type 2 diabetes (T2D). Most of them seem to influence the capacity of beta-cells to increase insulin secretion to meet the demands imposed by an increase in body weight and insulin resistance. This probably represents only the tip of the iceberg, and over the next few years refined tools will provide a more complete picture of the genetic complexity of T2D. This will not only include the current dissection of common variants increasing the susceptibility of the disease but also rare variants with stronger effects, copy number variations and epigenetic effects like DNA methylation and histone acetylation. For the first time, we can anticipate with some confidence 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
Diabetes, Obesity and Metabolism
volume
11 Suppl 4
pages
149 - 158
publisher
Wiley-Blackwell
external identifiers
  • wos:000270613000016
  • pmid:19817797
  • scopus:70350318770
ISSN
1462-8902
DOI
10.1111/j.1463-1326.2009.01117.x
language
English
LU publication?
yes
id
75adb567-9e2d-475d-b826-b0f34c47991a (old id 1500466)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/19817797?dopt=Abstract
date added to LUP
2009-11-03 14:33:25
date last changed
2017-10-01 04:58:38
@article{75adb567-9e2d-475d-b826-b0f34c47991a,
  abstract     = {Although the genetic causes of monogenic disorders have been successfully identified in the past, the success in dissecting the genetics of complex polygenic diseases has until now been limited. With the introduction of whole genome wide association studies (WGAS) in 2007, the picture has been dramatically changed. Today we know of about 20 genetic variants increasing the risk of type 2 diabetes (T2D). Most of them seem to influence the capacity of beta-cells to increase insulin secretion to meet the demands imposed by an increase in body weight and insulin resistance. This probably represents only the tip of the iceberg, and over the next few years refined tools will provide a more complete picture of the genetic complexity of T2D. This will not only include the current dissection of common variants increasing the susceptibility of the disease but also rare variants with stronger effects, copy number variations and epigenetic effects like DNA methylation and histone acetylation. For the first time, we can anticipate with some confidence that the genetics of a complex disease like T2D really can be dissected.},
  author       = {Groop, Leif and Lyssenko, Valeriya},
  issn         = {1462-8902},
  language     = {eng},
  pages        = {149--158},
  publisher    = {Wiley-Blackwell},
  series       = {Diabetes, Obesity and Metabolism},
  title        = {Genetic basis of beta-cell dysfunction in man.},
  url          = {http://dx.doi.org/10.1111/j.1463-1326.2009.01117.x},
  volume       = {11 Suppl 4},
  year         = {2009},
}