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DNA methylation as a diagnostic and therapeutic target in the battle against Type 2 diabetes.

Rönn, Tina LU and Ling, Charlotte LU orcid (2015) In Epigenomics 7(3). p.451-460
Abstract
Type 2 diabetes (T2D) develops due to insulin resistance and impaired insulin secretion, predominantly in genetically predisposed subjects exposed to nongenetic risk factors like obesity, physical inactivity and ageing. Emerging data suggest that epigenetics also play a key role in the pathogenesis of T2D. Genome-wide studies have identified altered DNA methylation patterns in pancreatic islets, skeletal muscle and adipose tissue from subjects with T2D compared with nondiabetic controls. Environmental factors known to affect T2D, including obesity, exercise and diet, have also been found to alter the human epigenome. Additionally, ageing and the intrauterine environment are associated with differential DNA methylation. Together, these data... (More)
Type 2 diabetes (T2D) develops due to insulin resistance and impaired insulin secretion, predominantly in genetically predisposed subjects exposed to nongenetic risk factors like obesity, physical inactivity and ageing. Emerging data suggest that epigenetics also play a key role in the pathogenesis of T2D. Genome-wide studies have identified altered DNA methylation patterns in pancreatic islets, skeletal muscle and adipose tissue from subjects with T2D compared with nondiabetic controls. Environmental factors known to affect T2D, including obesity, exercise and diet, have also been found to alter the human epigenome. Additionally, ageing and the intrauterine environment are associated with differential DNA methylation. Together, these data highlight a key role for epigenetics and particularly DNA methylation in the growing incidence of T2D. (Less)
Please use this url to cite or link to this publication:
author
and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Epigenomics
volume
7
issue
3
pages
451 - 460
publisher
Future Medicine Ltd.
external identifiers
  • pmid:26077431
  • wos:000356241700010
  • scopus:84931301395
  • pmid:26077431
ISSN
1750-192X
DOI
10.2217/epi.15.7
language
English
LU publication?
yes
id
86163a06-fefb-4c28-836a-510b2b1d8845 (old id 7476734)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/26077431?dopt=Abstract
date added to LUP
2016-04-01 10:16:53
date last changed
2022-08-20 01:19:11
@article{86163a06-fefb-4c28-836a-510b2b1d8845,
  abstract     = {{Type 2 diabetes (T2D) develops due to insulin resistance and impaired insulin secretion, predominantly in genetically predisposed subjects exposed to nongenetic risk factors like obesity, physical inactivity and ageing. Emerging data suggest that epigenetics also play a key role in the pathogenesis of T2D. Genome-wide studies have identified altered DNA methylation patterns in pancreatic islets, skeletal muscle and adipose tissue from subjects with T2D compared with nondiabetic controls. Environmental factors known to affect T2D, including obesity, exercise and diet, have also been found to alter the human epigenome. Additionally, ageing and the intrauterine environment are associated with differential DNA methylation. Together, these data highlight a key role for epigenetics and particularly DNA methylation in the growing incidence of T2D.}},
  author       = {{Rönn, Tina and Ling, Charlotte}},
  issn         = {{1750-192X}},
  language     = {{eng}},
  number       = {{3}},
  pages        = {{451--460}},
  publisher    = {{Future Medicine Ltd.}},
  series       = {{Epigenomics}},
  title        = {{DNA methylation as a diagnostic and therapeutic target in the battle against Type 2 diabetes.}},
  url          = {{https://lup.lub.lu.se/search/files/1711227/8820636}},
  doi          = {{10.2217/epi.15.7}},
  volume       = {{7}},
  year         = {{2015}},
}