DNA methylation as a diagnostic and therapeutic target in the battle against Type 2 diabetes.
Rönn, Tina LU and Ling, Charlotte LU
(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:
https://lup.lub.lu.se/record/7476734
- author
- Rönn, Tina
LU
and Ling, Charlotte
LU
- organization
- publishing date
- 2015
- 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}},
}