Genetic, nongenetic and epigenetic risk determinants in developmental programming of type 2 diabetes
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Genetic, nongenetic and epigenetic risk determinants in developmental programming of type 2 diabetes. / Vaag, Allan; Brøns, Charlotte; Gillberg, Linn; Hansen, Ninna S; Hjort, Line; Arora, Geeti P; Thomas, Nihal; Broholm, Christa; Ribel-Madsen, Rasmus; Grunnet, Louise G.
In: Acta Obstetrica et Gynecologica, Vol. 93, No. 11, 11.2014, p. 1099-1108.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Genetic, nongenetic and epigenetic risk determinants in developmental programming of type 2 diabetes
AU - Vaag, Allan
AU - Brøns, Charlotte
AU - Gillberg, Linn
AU - Hansen, Ninna S
AU - Hjort, Line
AU - Arora, Geeti P
AU - Thomas, Nihal
AU - Broholm, Christa
AU - Ribel-Madsen, Rasmus
AU - Grunnet, Louise G
N1 - © 2014 Nordic Federation of Societies of Obstetrics and Gynecology.
PY - 2014/11
Y1 - 2014/11
N2 - 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 prenatal and postnatal nongenetic factors, and it remains unknown to what 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 with nongenetic and epigenetic risk determinants and disease mechanisms.
AB - 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 prenatal and postnatal nongenetic factors, and it remains unknown to what 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 with nongenetic and epigenetic risk determinants and disease mechanisms.
KW - Adult
KW - Diabetes Mellitus, Type 2
KW - Diabetes, Gestational
KW - Epigenesis, Genetic
KW - Female
KW - Fetal Development
KW - Genetic Predisposition to Disease
KW - Humans
KW - Pregnancy
KW - Prenatal Exposure Delayed Effects
KW - Risk Factors
U2 - 10.1111/aogs.12494
DO - 10.1111/aogs.12494
M3 - Journal article
C2 - 25179736
VL - 93
SP - 1099
EP - 1108
JO - Acta Obstetricia et Gynecologica Scandinavica
JF - Acta Obstetricia et Gynecologica Scandinavica
SN - 0001-6349
IS - 11
ER -
ID: 137908020