Alterations in the hepatic epigenome in mice exposed to a maternal high fat diet in utero
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA310332 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Exposure to a high fat (HF) diet in utero is associated with increased incidence of cardiovascular disease, diabetes and metabolic syndrome later in life. However, the molecular basis of this enhanced susceptibility for metabolic disease is poorly understood. We performed genome-wide DNA methylation analysis to examine DNA methylation patterns in liver of offspring exposed to a Control or HF maternal diet. WT mice were fed a C (9.5% fat, 3.59 kcal/g) or HF (35.5% fat, 5.29 kcal/g) diet for 2 wk before mating, throughout pregnancy and lactation. Offspring were weaned to a low fat (5.6% fat, 3.4 kcal/g) diet and were sacrificed at 5wks of age. DNA methylation analysis revealed the majority of differentially methylated regions were hypermethylated in HF liver. Chromosomal distribution analysis showed hypermethylation hot spots on chromosomes 4 (atherosclerosis susceptibility QTL1) and 18 (insulin dependent susceptibility 21). Most of the hypermethylated genes in these hot spots are associated with cardiovascular system development and function. In summary, exposure to a maternal HF diet significantly alters the DNA methylation patterns in the liver of exposed offspring and contributes to programmed development of metabolic disease later in life.
2017-10-02 | GSE77430 | GEO
Project description:Exposure to a high fat (HF) diet in utero is associated with increased incidence of cardiovascular disease, diabetes and metabolic syndrome later in life. However, the molecular basis of this enhanced susceptibility for metabolic disease is poorly understood. We used gene expression microarray to examine mRNA expression patterns in liver of offspring exposed to a Control or HF maternal diet. WT mice were fed a Control (9.5% fat, 3.59 kcal/g) or HF (35.5% fat, 5.29 kcal/g) diet for 2 wk before mating, throughout pregnancy and lactation. Offspring were weaned to a low fat (5.6% fat, 3.4 kcal/g) diet and were sacrificed at 5wks of age. Exposure to a maternal HF milieu activated genes of immune response, inflammation, and hepatic dysfunction. Conversely genes of lipid metabolism and biogenesis were down regulated especially in the cholesterol biosynthesis pathway. In summary, exposure to a maternal HF diet significantly alters the gene expression patterns in the liver of exposed offspring and contributes to development of metabolic disease later in life.
2017-10-02 | GSE77431 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2017-10-02 | GSE77432 | GEO
Project description:Background: Maternal smoking during pregnancy is a major risk factor for adverse health outcomes. The main objective of the study was to assess the impact of in utero tobacco exposure on DNA methylation in children born at term with appropriate weight at birth. Methods: Twenty mother-newborn dyads, after uncomplicated pregnancies, in the absence of perinatal illness were included. All mothers were healthy with no cardiovascular risk factors, except for the associated risks among those mothers who smoked. Umbilical cord blood (for methylation arrays) and maternal peripheral venous blood (for cotine level measurement) were collected and an epigenome-wide association study was performed using a 450K epigenome-wide scan (Illumina Infinium HumanMethylation 450BeadChip) with adjustment to normalize the DNA methylation for data cell variability in whole blood. Results: The maternal plasmatic cotinine levels ranged from 10.70-115.40 ng/ml in the exposed group to 0-0.59 ng/ml in the non-exposed group. After adjusting for multiple comparisons in 427102 probes, statistically significant differences for 31 CpG sites, associated to 25 genes were observed. There was a greater than expected proportion of statistically-significant loci located in CpG islands (FisherM-bM-^@M-^Ys exact test, p=0.029) and of those CpG islands, 90.3% exhibit higher methylation levels in the exposed group. The most striking and significant CpG site, cg05727225, is located in the chromosome 11p15.4, within the adrenomedullin gene. Conclusions: In utero tobacco exposure, even in the absence of fetal growth restriction, may alter the epigenome, contributing to global DNA hypomethylation. Therefore, DNA status can be used as a biomarker of prenatal insults. Considering the possibility to reverse epigenetic modifications, a window of opportunity exists to change the programmed chronic disease. Twenty mother-newborn dyads, after uncomplicated pregnancies, in the absence of perinatal illness were included. All mothers were healthy with no cardiovascular risk factors, except for the associated risks among those mothers who smoked. Umbilical cord blood were collected and an epigenome-wide association study was performed using a 450K epigenome-wide scan (Illumina Infinium HumanMethylation 450BeadChip) with adjustment to normalize the DNA methylation for data cell variability in whole blood.
2015-02-16 | E-GEOD-64316 | biostudies-arrayexpress
Project description:Epidemiologic studies have clearly identified modifications of fetal environment as a risk factor for the development of cardiovascular diseases and of metabolic syndrome in adulthood. In our experimental model, rats exposed to maternal diabetes develop a volume-dependent hypertension as early as 6 month of age. In order to determine if the development of hypertension results from an abnormal vascular fetal programming, gene expression profile of thoracic aorta were studied in adult rats exposed in utero to maternal hyperglycemia.
2010-02-01 | GSE16750 | GEO
Project description:Background: Maternal smoking during pregnancy is a major risk factor for adverse health outcomes. The main objective of the study was to assess the impact of in utero tobacco exposure on DNA methylation in children born at term with appropriate weight at birth. Methods: Twenty mother-newborn dyads, after uncomplicated pregnancies, in the absence of perinatal illness were included. All mothers were healthy with no cardiovascular risk factors, except for the associated risks among those mothers who smoked. Umbilical cord blood (for methylation arrays) and maternal peripheral venous blood (for cotine level measurement) were collected and an epigenome-wide association study was performed using a 450K epigenome-wide scan (Illumina Infinium HumanMethylation 450BeadChip) with adjustment to normalize the DNA methylation for data cell variability in whole blood. Results: The maternal plasmatic cotinine levels ranged from 10.70-115.40 ng/ml in the exposed group to 0-0.59 ng/ml in the non-exposed group. After adjusting for multiple comparisons in 427102 probes, statistically significant differences for 31 CpG sites, associated to 25 genes were observed. There was a greater than expected proportion of statistically-significant loci located in CpG islands (Fisher’s exact test, p=0.029) and of those CpG islands, 90.3% exhibit higher methylation levels in the exposed group. The most striking and significant CpG site, cg05727225, is located in the chromosome 11p15.4, within the adrenomedullin gene. Conclusions: In utero tobacco exposure, even in the absence of fetal growth restriction, may alter the epigenome, contributing to global DNA hypomethylation. Therefore, DNA status can be used as a biomarker of prenatal insults. Considering the possibility to reverse epigenetic modifications, a window of opportunity exists to change the programmed chronic disease.
2015-02-16 | GSE64316 | GEO
Project description:Exposure to intrauterine heat stress during late gestation affects offspring performance into adulthood. However, underlying mechanistic links between thermal insult in fetal life and postnatal outcomes are not completely understood. Utilizing RNA Sequencing, this study characterized the mammary gland transcriptome of heifers that were gestated under maternal conditions of heat stress or cooling, i.e., in utero heat stressed (HT) vs. in utero cooled (CL). Mammary tissues were collected from three HT and three CL heifers during their first lactation.
2018-08-30 | GSE119216 | GEO
Project description:In utero heat stress alters the offspring epigenome
| PRJNA488483 | ENA
Project description:Exposure to intrauterine heat stress during late gestation affects offspring performance into adulthood. However, underlying mechanistic links between thermal insult in fetal life and postnatal outcomes are not completely understood. Utilizing Reduced Representation Bisulfite Sequencing, this study evaluated DNA methylation of liver and mammary gland of bull calves and heifers that were gestated under maternal conditions of heat stress or cooling, i.e., in utero heat stressed (HT) vs. in utero cooled (CL). Liver samples from bull calves (CT = 5 and HT = 4) were collected at birth while mammary gland samples from heifers (CT = 3 and HT = 3) were collected during their first lactation.
2018-09-05 | GSE119445 | GEO
Project description:In utero heat stress alters the offspring epigenome [methylation]
| PRJNA489263 | ENA