Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification and Comparative Analyses of Myocardial miRNAs Involved in Fetal Response to Maternal Obesity

ABSTRACT: Maternal obesity programs the offspring to cardiovascular disease, insulin resistance, and obesity. We sequenced and profiled the cardiac miRNAs that were dysregulated in the hearts of baboon fetuses born to a high fat / high fructose diet fed mothers compared to a regular diet fed mothers.

ORGANISM(S): Papio hamadryas

PROVIDER: GSE43323 | GEO | 2013/02/01

SECONDARY ACCESSION(S): PRJNA185430

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Identification and Comparative Analyses of Myocardial miRNAs Involved in Fetal Response to Maternal Obesity

Project description:Maternal obesity programs the offspring to cardiovascular disease, insulin resistance, and obesity. We sequenced and profiled the cardiac miRNAs that were dysregulated in the hearts of baboon fetuses born to a high fat / high fructose diet fed mothers compared to a regular diet fed mothers. Fetal hearts were collected from baboon fetuses born to obese and lean mothers, total RNA was isolated, and fetal cardiac miRNA were sequenced and profiled

2013-02-01 | E-GEOD-43323 | biostudies-arrayexpress

Identification and Comparative Analyses of Myocardial miRNAs Involved in Fetal Response to Maternal Undernutrition

Project description:Poor maternal nutrition during pregnancy causes intrauterine growth retardation, which, in turn, is associated with increased risk of cardiovascular and metabolic diseases in later life Fetal hearts were collected from baboon fetuses born to regularly fed and undernurished mothers. Total RNA was isolated, and fetal cardiac miRNA were profiled

2015-11-02 | E-GEOD-69609 | biostudies-arrayexpress

Depot-dependent effects of maternal nutrient restriction on baboon fetal preadipocyte global gene profiles

Project description:Suboptimal intrauterine nutrition predisposes the fetus to central obesity and metabolic syndrome in adult life, suggesting nutritional programming of the fat distribution. However, the underlying mechanisms are not elucidated. We hypothesized that prenatal nutritional deprivation leads to stimulation of adipogenesis, as an adaptive mechanism, in a depot-dependent manner. The induction of adipogenesis is most enhanced in the subcutaneous lower-body depots, followed by the subcutaneous upper-body and visceral adipose tissue depots. Stimulation of adipogenesis may lead to an early consumption of the stem cell pool, and thus, may impair adipose tissue expandability postnatally, which may lead to differences in regional adipose tissue growth. We tested this hypothesis by analyzing global gene expression to identify expression patterns in subcutaneous abdominal, subcutaneous femoral, and omental adipose depots of baboon fetuses that have been altered by nutritional maternal deprivation. Adipose tissue was collected from baboon fetuses at 165 dG from mothers fed control or 30% nutrient-restricted diets (three females and one male in each group). 24 samples, each consisted of pooled total RNA from triplicate wells (6-well plate).

2011-12-16 | E-GEOD-34464 | biostudies-arrayexpress

Depot-dependent effects of maternal nutrient restriction on baboon fetal preadipocyte global gene profiles

2011-12-16 | GSE34464 | GEO

Transcriptomics of rat born to dams fed a diet deficient in methyl group donors

Project description:It is clearly established that the maternal diet during pregnancy can induce physiological and metabolic adaptations in the developing fetus which determine its susceptibility later in life to develop diabetes, obesity... The molecular and genomic mechanisms underlying the programming of the metabolic syndrome remain largely unknown but may involve resetting of epigenetic marks and fetal gene expression. We analyzed the profile of the liver transcriptome in 21-day-old rats born to mothers fed with a standard diet or a diet lacking methyl donor nutrients (Vitamin B12 and folates) during gestation and lactation. From a total of 44,000 probes for 26,456 genes, we found two gene clusters whose expression levels had statistically significant differences between control and deficient rats: 3,269 up-regulated and 2,841 down-regulated genes. Bioinformatics analysis revealed that these genes are mainly involved in glucose and lipid metabolism, nervous system, coagulation, endoplasmic reticulum (ER) stress and mitochondrial function. Modifications of gene expression in rat liver were measured in 21-day-old rats born to mothers fed with a standard diet or a diet lacking methyl donor nutrients (Vitamin B12 and folates). Eight independent experiments were performed (4 Controls versus 4 Methyl Donor Deficiency - MDD).

2015-06-22 | E-GEOD-59039 | biostudies-arrayexpress

Are you also what Your Mother Eats? Distinct Proteomic Portrait as a Result of Maternal High-Fat Diet in the Cerebral Cortex of the Adult Mouse.

Project description:Background: Epidemiological studies suggest an association between maternal obesity and adverse neurodevelopmental outcomes in offspring. Objective: To compare the global proteomic portrait in the cerebral cortex between mice born to mothers on a high-fat or control diet who themselves were fed a high-fat or control diet. Methods: Male mice born to dams fed a control (C) or high fat (H) diet four weeks before conception and during gestation and lactation were assigned to either C or H diet at weaning. Mice (n=24) were sacrificed at 19-weeks and their cerebral cortices were pooled into 8 samples and analysed using an iTRAQ based 2D LC-MS methodology. Results: A total of 6,695 proteins were identified and fully quantified (q<0.01). Approximately 10% of these proteins demonstrated a minimum of one Standard Deviation of regulation across all biological replicates in at least one of the experimental groups (CH, HC, HH) relative to the control (CC). Principal component analysis and hierarchical clustering analysis showed that mice clustered based on the diet of the mother and not their current diet. In silico bioinformatics analysis revealed that maternal high-fat diet was significantly associated with response to hypoxia/oxidative stress and apoptosis in the cerebral cortex of the adult offspring. Conclusion: Maternal high-fat diet was associated with distinct endophenotypic changes of the adult mouse cerebral cortex independent of the diet of the offspring. The identified modulated proteins could represent novel therapeutic targets for the prevention of neuropathological features resulting from maternal obesity.

2018-01-29 | PXD001540 | Pride

Epigenomics of rat born to dams fed a diet deficient in methyl group donors (MDD)

Project description:It is clearly established that the maternal diet during pregnancy can induce physiological and metabolic adaptations in the developing fetus which determine its susceptibility later in life to develop diabetes, obesity... The molecular and genomic mechanisms underlying the programming of the metabolic syndrome remain largely unknown but may involve resetting of epigenetic marks and fetal gene expression. We analyzed the profile of the liver methylome in 21-day-old rats born to mothers fed with a standard diet or a diet lacking methyl donor nutrients (Vitamin B12 and folates) during gestation and lactation. Modifications of DNA methylation were found in the promoter regions of 1,032 genes out of 14,981 genes. Bioinformatics analysis revealed that these genes are mainly involved in glucose and lipid metabolism, nervous system, coagulation, endoplasmic reticulum (ER) stress and mitochondrial function. MDD induced modifications of methylation in rat liver were measured in 21-day-old rats born to dams fed with standard food or food deficient in methyl group donor. Six independent experiments were performed (3 controls versus 3 MDD).

2015-06-22 | E-GEOD-59191 | biostudies-arrayexpress

Proteomics of liver from mice fed high fat diet (HFD) or regular chow diet

Project description:Proteomics of liver tissue from mice fed a high fat diet (HFD) or regular chow diet. Data accompany our paper entitled “Dynamic Regulation of N6,2′-O-dimethyladenosine (m6Am) in Obesity” scheduled for publication in Nature Communications, 2021

2021-10-27 | PXD029280 | Pride

Gene expression altered by high-fructose diet feeding and Chrebp deficiency

Project description:Epidemiologic and animal studies implicate overconsumption of fructose in the development of non-alcoholic fatty liver disease, but the molecular mechanisms underlying fructose-induced chronic liver diseases remains largely unknown. We present evidence supporting the essential function of the lipogenic transcription factor ChREBP in mediating adaptation response to fructose and protecting against fructose-induced hepatotoxicity. High-fructose diet (HFrD) activates hepatic lipogenesis via a ChREBP-dependent manner in wildtype mice, while inducing steatohepatitis in Chrebp-KO mice. In Chrebp-KO mouse livers, HFrD reduces levels of molecular chaperones and activates the CHOP-dependent unfolded protein response, whereas administration of chemical chaperone or Chop shRNA rescues liver injury. Gene expression profiling revealed elevated expression of cholesterol biosynthesis genes in Chrebp-KO livers after HFrD, in parallel with increased abundance of nuclear SREBP2. genes expression were compared between livers of wildtype mice fed 70%-fructose-diet v.s. regular chow, and between livers of Chrebp-/- mice v.s. wildtype mice fed 70%-fructose-diet.

2017-03-21 | GSE96820 | GEO

GDF15 reduces NAFLD through mechanisms that are independent of the suppression of food intake

Project description:The effects of recombinant human GDF15 and matched caloric restriction in pair-fed controls on obesity and NAFLD in mice fed western diet high in both fat and fructose and housed at thermoneutrality (TN, 29 °C).

2023-04-14 | GSE229708 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data