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DNA methylation and gene expression of TXNIP in adult offspring of women with diabetes in pregnancy

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@article{f0e7f9ac50a1480f82321282e1788ef0,
title = "DNA methylation and gene expression of TXNIP in adult offspring of women with diabetes in pregnancy",
abstract = "BACKGROUND: Fetal exposure to maternal diabetes increases the risk of type 2 diabetes (T2DM), possibly mediated by epigenetic mechanisms. Low blood TXNIP DNA methylation has been associated with elevated glucose levels and risk of T2DM, and increased skeletal muscle TXNIP gene expression was reported in subjects with impaired glucose metabolism or T2DM. Subcutaneous adipose tissue (SAT) and skeletal muscle play a key role in the control of whole body glucose metabolism and insulin action. The extent to which TXNIP DNA methylation levels are decreased and/or gene expression levels increased in SAT or skeletal muscle of a developmentally programmed at-risk population is unknown.OBJECTIVE AND METHODS: The objective of this study was to investigate TXNIP DNA methylation and gene expression in SAT and skeletal muscle, and DNA methylation in blood, from adult offspring of women with gestational diabetes (O-GDM, n = 82) or type 1 diabetes (O-T1DM, n = 67) in pregnancy compared with offspring of women from the background population (O-BP, n = 57).RESULTS: SAT TXNIP DNA methylation was increased (p = 0.032) and gene expression decreased (p = 0.001) in O-GDM, but these differences were attenuated after adjustment for confounders. Neither blood/muscle TXNIP DNA methylation nor muscle gene expression differed between groups.CONCLUSION: We found no evidence of decreased TXNIP DNA methylation or increased gene expression in metabolic target tissues of offspring exposed to maternal diabetes. Further studies are needed to confirm and understand the paradoxical SAT TXNIP DNA methylation and gene expression changes in O-GDM subjects.",
keywords = "Journal Article",
author = "Azadeh Houshmand-Oeregaard and Line Hjort and Louise Kelstrup and Hansen, {Ninna S} and Christa Broholm and Linn Gillberg and Clausen, {Tine D} and Mathiesen, {Elisabeth R} and Peter Damm and Allan Vaag",
year = "2017",
doi = "10.1371/journal.pone.0187038",
language = "English",
volume = "12",
pages = "e0187038",
journal = "P L o S One",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "10",

}

RIS

TY - JOUR

T1 - DNA methylation and gene expression of TXNIP in adult offspring of women with diabetes in pregnancy

AU - Houshmand-Oeregaard, Azadeh

AU - Hjort, Line

AU - Kelstrup, Louise

AU - Hansen, Ninna S

AU - Broholm, Christa

AU - Gillberg, Linn

AU - Clausen, Tine D

AU - Mathiesen, Elisabeth R

AU - Damm, Peter

AU - Vaag, Allan

PY - 2017

Y1 - 2017

N2 - BACKGROUND: Fetal exposure to maternal diabetes increases the risk of type 2 diabetes (T2DM), possibly mediated by epigenetic mechanisms. Low blood TXNIP DNA methylation has been associated with elevated glucose levels and risk of T2DM, and increased skeletal muscle TXNIP gene expression was reported in subjects with impaired glucose metabolism or T2DM. Subcutaneous adipose tissue (SAT) and skeletal muscle play a key role in the control of whole body glucose metabolism and insulin action. The extent to which TXNIP DNA methylation levels are decreased and/or gene expression levels increased in SAT or skeletal muscle of a developmentally programmed at-risk population is unknown.OBJECTIVE AND METHODS: The objective of this study was to investigate TXNIP DNA methylation and gene expression in SAT and skeletal muscle, and DNA methylation in blood, from adult offspring of women with gestational diabetes (O-GDM, n = 82) or type 1 diabetes (O-T1DM, n = 67) in pregnancy compared with offspring of women from the background population (O-BP, n = 57).RESULTS: SAT TXNIP DNA methylation was increased (p = 0.032) and gene expression decreased (p = 0.001) in O-GDM, but these differences were attenuated after adjustment for confounders. Neither blood/muscle TXNIP DNA methylation nor muscle gene expression differed between groups.CONCLUSION: We found no evidence of decreased TXNIP DNA methylation or increased gene expression in metabolic target tissues of offspring exposed to maternal diabetes. Further studies are needed to confirm and understand the paradoxical SAT TXNIP DNA methylation and gene expression changes in O-GDM subjects.

AB - BACKGROUND: Fetal exposure to maternal diabetes increases the risk of type 2 diabetes (T2DM), possibly mediated by epigenetic mechanisms. Low blood TXNIP DNA methylation has been associated with elevated glucose levels and risk of T2DM, and increased skeletal muscle TXNIP gene expression was reported in subjects with impaired glucose metabolism or T2DM. Subcutaneous adipose tissue (SAT) and skeletal muscle play a key role in the control of whole body glucose metabolism and insulin action. The extent to which TXNIP DNA methylation levels are decreased and/or gene expression levels increased in SAT or skeletal muscle of a developmentally programmed at-risk population is unknown.OBJECTIVE AND METHODS: The objective of this study was to investigate TXNIP DNA methylation and gene expression in SAT and skeletal muscle, and DNA methylation in blood, from adult offspring of women with gestational diabetes (O-GDM, n = 82) or type 1 diabetes (O-T1DM, n = 67) in pregnancy compared with offspring of women from the background population (O-BP, n = 57).RESULTS: SAT TXNIP DNA methylation was increased (p = 0.032) and gene expression decreased (p = 0.001) in O-GDM, but these differences were attenuated after adjustment for confounders. Neither blood/muscle TXNIP DNA methylation nor muscle gene expression differed between groups.CONCLUSION: We found no evidence of decreased TXNIP DNA methylation or increased gene expression in metabolic target tissues of offspring exposed to maternal diabetes. Further studies are needed to confirm and understand the paradoxical SAT TXNIP DNA methylation and gene expression changes in O-GDM subjects.

KW - Journal Article

U2 - 10.1371/journal.pone.0187038

DO - 10.1371/journal.pone.0187038

M3 - Journal article

VL - 12

SP - e0187038

JO - P L o S One

JF - P L o S One

SN - 1932-6203

IS - 10

ER -

ID: 51981081