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Genetic, non-genetic and epigenetic risk determinants in developmental programming of type 2 diabetes.

Vaag, Allan LU ; Brøns, Charlotte; Gillberg, Linn LU ; Hansen, Ninna S; Hjort, Line; Arora, Geeti LU ; Thomas, Nihal; Broholm, Christa; Ribel-Madsen, Rasmus and Grunnet, Louise G (2014) In Acta Obstetricia et Gynecologica Scandinavica 93(11). p.1099-1108
Abstract
Low birthweight (LBW) individuals and offspring of women with gestational diabetes mellitus (GDM) exhibit increased risk of developing type 2 diabetes (T2D) and associated cardiometabolic traits in adulthood, which for both groups may be mediated by adverse events and developmental changes in fetal life. T2D is a multifactorial disease occurring as a result of complicated interplay between genetic and both pre- as well as postnatal non-genetic factors, and it remains unknown to which extent the increased risk of T2D associated with LBW or GDM in the mother may be due to, or confounded by, genetic factors. Indeed, it has been shown that genetic changes influencing risk of diabetes may also be associated with reduced fetal growth as a result... (More)
Low birthweight (LBW) individuals and offspring of women with gestational diabetes mellitus (GDM) exhibit increased risk of developing type 2 diabetes (T2D) and associated cardiometabolic traits in adulthood, which for both groups may be mediated by adverse events and developmental changes in fetal life. T2D is a multifactorial disease occurring as a result of complicated interplay between genetic and both pre- as well as postnatal non-genetic factors, and it remains unknown to which extent the increased risk of T2D associated with LBW or GDM in the mother may be due to, or confounded by, genetic factors. Indeed, it has been shown that genetic changes influencing risk of diabetes may also be associated with reduced fetal growth as a result of reduced insulin secretion and/or action. Similarly, increased risk of T2D among offspring could be explained by T2D susceptibility genes shared between the mother and her offspring. Epigenetic mechanisms may explain the link between factors operating in fetal life and later risk of developing T2D, but so far convincing evidence is lacking for epigenetic changes as a prime and direct cause of T2D. This review addresses recent literature on the early origins of adult disease hypothesis, with a special emphasis on the role of genetic compared to non-genetic and epigenetic risk determinants and disease mechanisms. This article is protected by copyright. All rights reserved. (Less)
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author
organization
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type
Contribution to journal
publication status
published
subject
in
Acta Obstetricia et Gynecologica Scandinavica
volume
93
issue
11
pages
1099 - 1108
publisher
Wiley-Blackwell
external identifiers
  • pmid:25179736
  • wos:000344228200007
  • scopus:84912037167
ISSN
1600-0412
DOI
10.1111/aogs.12494
language
English
LU publication?
yes
id
e7833b17-18a0-48f1-8930-a87d96ae55f4 (old id 4692551)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/25179736?dopt=Abstract
date added to LUP
2014-10-01 12:39:50
date last changed
2017-10-01 03:04:39
@article{e7833b17-18a0-48f1-8930-a87d96ae55f4,
  abstract     = {Low birthweight (LBW) individuals and offspring of women with gestational diabetes mellitus (GDM) exhibit increased risk of developing type 2 diabetes (T2D) and associated cardiometabolic traits in adulthood, which for both groups may be mediated by adverse events and developmental changes in fetal life. T2D is a multifactorial disease occurring as a result of complicated interplay between genetic and both pre- as well as postnatal non-genetic factors, and it remains unknown to which extent the increased risk of T2D associated with LBW or GDM in the mother may be due to, or confounded by, genetic factors. Indeed, it has been shown that genetic changes influencing risk of diabetes may also be associated with reduced fetal growth as a result of reduced insulin secretion and/or action. Similarly, increased risk of T2D among offspring could be explained by T2D susceptibility genes shared between the mother and her offspring. Epigenetic mechanisms may explain the link between factors operating in fetal life and later risk of developing T2D, but so far convincing evidence is lacking for epigenetic changes as a prime and direct cause of T2D. This review addresses recent literature on the early origins of adult disease hypothesis, with a special emphasis on the role of genetic compared to non-genetic and epigenetic risk determinants and disease mechanisms. This article is protected by copyright. All rights reserved.},
  author       = {Vaag, Allan and Brøns, Charlotte and Gillberg, Linn and Hansen, Ninna S and Hjort, Line and Arora, Geeti and Thomas, Nihal and Broholm, Christa and Ribel-Madsen, Rasmus and Grunnet, Louise G},
  issn         = {1600-0412},
  language     = {eng},
  number       = {11},
  pages        = {1099--1108},
  publisher    = {Wiley-Blackwell},
  series       = {Acta Obstetricia et Gynecologica Scandinavica},
  title        = {Genetic, non-genetic and epigenetic risk determinants in developmental programming of type 2 diabetes.},
  url          = {http://dx.doi.org/10.1111/aogs.12494},
  volume       = {93},
  year         = {2014},
}