Levels of maternal care in dogs affect adult offspring temperament.
Ontology highlight
ABSTRACT:
SUBMITTER: Foyer P
PROVIDER: S-EPMC4725833 | biostudies-other | 2016 Jan
REPOSITORIES: biostudies-other
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Project description:Aims/hypothesisDuring pregnancy, maternal metabolic disease and hormonal imbalance may alter fetal beta cell development and/or proliferation, thus leading to an increased risk for developing type 2 diabetes in adulthood. Although thyroid hormones play an important role in fetal endocrine pancreas development, the impact of maternal hypothyroidism on glucose homeostasis in adult offspring remains poorly understood.MethodsWe investigated this using a mouse model of hypothyroidism, induced by administration of an iodine-deficient diet supplemented with propylthiouracil during gestation.ResultsHere, we show that, when fed normal chow, adult mice born to hypothyroid mothers were more glucose-tolerant due to beta cell hyperproliferation (two- to threefold increase in Ki67-positive beta cells) and increased insulin sensitivity. However, following 8 weeks of high-fat feeding, these offspring gained 20% more body weight, became profoundly hyperinsulinaemic (with a 50% increase in fasting insulin concentration), insulin-resistant and glucose-intolerant compared with controls from euthyroid mothers. Furthermore, altered glucose metabolism was maintained in a second generation of animals.Conclusions/interpretationTherefore, gestational hypothyroidism induces long-term alterations in endocrine pancreas function, which may have implications for type 2 diabetes prevention in affected individuals.
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Project description:BackgroundEating disorders (ED) are chronic psychiatric disorders, common amongst women of reproductive age. ED in pregnancy are associated with poor nutrition and abnormal intrauterine growth. Increasing evidence also shows offspring of women with ED have adverse developmental and birth outcomes. We sought to carry out the first study investigating DNA methylation in offspring of women with ED. We compared cord blood DNA methylation in offspring of women with active ED (n = 21), past ED (n = 43) and age- and social class-matched controls (n = 126) as part of the Avon Longitudinal Study of Parents and Children.ResultsOffspring of women with both active and past ED had lower whole-genome methylation compared to controls (active ED 49.1% (95% confidence intervals 50.5-47.7%), past ED 49.2% (95% CI 50.7-47.7.0%), controls 52.4% (95% CI 53.0%-51.0%)). Amongst offspring of ED women, those born to women with restrictive-type and purging-type ED had lower methylation levels compared to those of controls. Offspring of women with an active restrictive ED in pregnancy had lower whole-genome methylation compared to offspring of women with past restrictive ED. We observed decreased methylation at the DHCR24 locus in offspring of women with active pregnancy ED (effect size (ES) = - 0.124, p = 6.94 × 10-8) and increased methylation at the LGALS2 locus in offspring of women with past ED (ES = 0.07, p = 3.74 × 10-7) compared to controls.ConclusionsMaternal active and past ED are associated with differences in offspring whole-genome methylation. Our results show altered DNA methylation in loci relevant to metabolism; these might be biomarkers of disrupted metabolic pathways in offspring of ED mothers. Further work is needed to examine potential mechanisms and functional outcomes of the observed methylation patterns.
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Project description:This SuperSeries is composed of the following subset Series: GSE20714: Broad epigenetic signature of maternal care in the brain of adult rats (DNA methylation and H3K9 acetylation profiles) GSE20717: Broad epigenetic signature of maternal care in the brain of adult rats (expression) Refer to individual Series
2011-03-09 | E-GEOD-20840 | biostudies-arrayexpress