Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Sex-specific programming effects of parental obesity in pre-implantation embryonic development_Microarray data on blastocyst transcriptomes

ABSTRACT: Obesity is a global rising problem with epidemiological dimension. Obese parents can have programming effects on their offspring leading to obesity and associated diseases in later life. This constitutes a vicious circle. Epidemiological data and studies in rodents demonstrated differential programming effects in male and female offspring, but the timing of their developmental origin is not known. This study investigated if sex-specific programming effects of parental obesity can already be detected in the pre-implantation period. Diet induced obese male or female mice were mated with normal-weight partners and blastocysts were recovered. Gene expression profiling revealed sex-specific responses of the blastocyst transcriptome to maternal and paternal obesity. The changes in the transcriptome of male blastocysts were more pronounced than those of female blastocysts, with a stronger impact of paternal than of maternal obesity. The sperm of obese mice revealed an increased abundance of several miRNAs compared to lean mice. Our study indicates that sex-specific programming effects of parental obesity already start in the pre‑implantation period and reveals specific alterations of the sperm miRNA profile as mechanistic link to programming effects of paternal obesity. We used microarrays to analyze the transcriptomes of sex-sorted blastocysts of mice, with one parent (either mother or father) being obese at the time of conception and compared it to the transcriptome of blasocysts of peri-conceptionally lean parents.

ORGANISM(S): Mus musculus

PROVIDER: GSE133767 | GEO | 2019/07/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Sex-specific programming effects of parental obesity in pre-implantation embryonic development [RNASeq Data of Sperm]

Project description:Obesity is a global rising problem with epidemiological dimension. Obese parents can have programming effects on their offspring leading to obesity and associated diseases in later life. This constitutes a vicious circle. Epidemiological data and studies in rodents demonstrated differential programming effects in male and female offspring, but the timing of their developmental origin is not known. This study investigated if sex-specific programming effects of parental obesity can already be detected in the pre-implantation period. Diet induced obese male or female mice were mated with normal-weight partners and blastocysts were recovered. Gene expression profiling revealed sex-specific responses of the blastocyst transcriptome to maternal and paternal obesity. The changes in the transcriptome of male blastocysts were more pronounced than those of female blastocysts, with a stronger impact of paternal than of maternal obesity. The sperm of obese mice revealed an increased abundance of several miRNAs compared to lean mice. Our study indicates that sex-specific programming effects of parental obesity already start in the pre‑implantation period and reveals specific alterations of the sperm miRNA profile as mechanistic link to programming effects of paternal obesity.

2019-07-07 | GSE133915 | GEO

Sex-specific programming effects of parental obesity in pre-implantation embryonic development [RNASeq Data of Oocytes]

2019-07-07 | GSE133914 | GEO

Genome-wide analysis reveals DNA methylation markers that varies with both age and obesity

Project description:Background: The obesity epidemic and the aging population of many western countries together with their associated diseases are major challenges for the healthcare. As obesity is a risk factor for many age related diseases, such as cancer, it is of importance to understand their interaction and the underlying molecular mechanisms. Lately, epigenetic programming in the form of DNA methylation and have been recognized for its importance in aging, obesity and several diseases. Method: Herein, the methylation level was determined for around 27000 CpG-islands in 46 DNA samples from adult peripheral blood with microarrays. The dependence for each CpG island with age, obesity and their interaction was ascertained with a general linear model. Results: The methylation level of more than 100 genomic sites were significantly altered with increasing age together with 10 additional sites that were differentially methylated with age in obese and lean individuals. The majority of the genomic sites were hypermethylated during aging, including the telomerase catalytic subunit (TERT). However, age dependent hypermethylation was prohibited or reverted in 8 of 10 regions in obese where an interaction between age and obesity was observed. Moreover, one region (LINC00304) was differentially methylated in obese and lean. Conclusion: This study provides evidence for an obesity influence on age driven epigenetic changes, which provide a molecular link between aging and obesity. This link and the identified markers may prove to be valuable biomarkers for the understanding of the molecular basis of aging, obesity and associated diseases. Bisulphite converted DNA from the 24 obese and 22 lean women were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2

2014-07-09 | E-GEOD-44763 | biostudies-arrayexpress

Effects of dietary obesity in fathers on gene expression of islets in the female offspring

Project description:The global prevalence of obesity is increasing across age and gender. The rising burden of obesity in young people contributes to the early emergence of type 2 diabetes. Having one parent obese is an independent risk factor for childhood obesity. While the detrimental impact of diet-induced maternal obesity on offspring is well established, the extent of the contribution of obese fathers is unclear, as is the role of non-genetic factors in the casual pathway. Here we show that paternal high fat diet exposure programmed β-cell ‘dysfunction’ in their F1 female offspring. Chronic high fat diet consumption in Sprague Dawley fathers led to increased body weight, adiposity, impaired glucose tolerance and insulin sensitivity. Relative to controls, their female offspring had lower body weight at day-1, increased pubertal growth rate, impaired insulin secretion and glucose tolerance, in the absence of obesity or increased adiposity. Paternal high fat diet was observed to alter gene expression of pancreatic islet genes in adult female offspring (P < 0.001); affected functional clusters includes calcium ion binding, insulin, apoptosis, Wnt and cell cycle organ/system development. This is the first reported study in mammals describing non-genetic, intergenerational transmission of metabolic sequelae of high fat diet from father to offspring. These findings support a role of fathers in metabolic programming of offspring and form a framework for further studies.

2010-10-21 | GSE19877 | GEO

DNA methylation covariation in human whole blood and sperm

Project description:Epidemiological studies in humans suggest that acquired paternal traits, such as obesity, are associated with a higher risk of fathering small for gestational age offspring. Studies in non-human mammals suggest that such associations could be mediated by DNA methylation changes in spermatozoa that influence offspring development in utero. Human obesity is associated with differential DNA methylation in peripheral blood. It is unclear, however, whether this differential DNA methylation is reflected in less readily available tissues such as spermatozoa. In this study, we profiled genome-wide DNA methylation with the Infinium MethylationEPIC array in matched samples of human blood and sperm from lean (discovery n = 47; replication n = 21) and obese (n = 22) healthy males of proven fertility. To characterize sperm-specific DNA methylation signatures, we compared spermatozoal DNA methylation data to that of nearly 6,000 somatic tissue samples available on the Gene Expression Omnibus database. We studied covariation patterns between whole blood and sperm and investigated consistent obesity-associated DNA methylation differences.

2020-05-03 | GSE149318 | GEO

Effects of dietary obesity in fathers on gene expression of fat in the female offspring (miRNA data)

Project description:The global prevalence of obesity is increasing across age and gender. The rising burden of obesity in young people contributes to the early emergence of type 2 diabetes. Having one parent obese is an independent risk factor for childhood obesity. While the detrimental impact of diet-induced maternal obesity on offspring is well established, the extent of the contribution of obese fathers is unclear, as is the role of non-genetic factors in the casual pathway. Here we show that paternal high fat diet exposure programmed β-cell ‘dysfunction’ in their F1 female offspring. Chronic high fat diet consumption in Sprague Dawley fathers led to increased body weight, adiposity, impaired glucose tolerance and insulin sensitivity. Relative to controls, their female offspring had lower body weight at day-1, increased pubertal growth rate, impaired insulin secretion and glucose tolerance, in the absence of obesity or increased adiposity. Paternal high fat diet altered the expression of 211 pancreatic islet genes in adult female offspring (P < 0.001); genes belonged to 8 functional clusters, including calcium ion binding, primary metabolic processes and ATP binding, and organ/system development. Broader KEGG pathway analysis of 2014 genes differentially expressed at the P < 0.01 level further demonstrated involvement of insulin and calcium signaling, and MAPK pathways. This is the first reported study in mammals describing non-genetic, intergenerational transmission of metabolic sequelae of high fat diet from father to offspring. These findings support a role of fathers in metabolic programming of offspring and form a framework for further studies.

2021-12-29 | GSE33559 | GEO

Effects of dietary obesity in fathers on gene expression of fat in the female offspring (mRNA data)

Project description:The global prevalence of obesity is increasing across age and gender. The rising burden of obesity in young people contributes to the early emergence of type 2 diabetes. Having one parent obese is an independent risk factor for childhood obesity. While the detrimental impact of diet-induced maternal obesity on offspring is well established, the extent of the contribution of obese fathers is unclear, as is the role of non-genetic factors in the casual pathway. Here we show that paternal high fat diet exposure programmed β-cell ‘dysfunction’ in their F1 female offspring. Chronic high fat diet consumption in Sprague Dawley fathers led to increased body weight, adiposity, impaired glucose tolerance and insulin sensitivity. Relative to controls, their female offspring had lower body weight at day-1, increased pubertal growth rate, impaired insulin secretion and glucose tolerance, in the absence of obesity or increased adiposity. Paternal high fat diet altered the expression of 211 pancreatic islet genes in adult female offspring (P < 0.001); genes belonged to 8 functional clusters, including calcium ion binding, primary metabolic processes and ATP binding, and organ/system development. Broader KEGG pathway analysis of 2014 genes differentially expressed at the P < 0.01 level further demonstrated involvement of insulin and calcium signaling, and MAPK pathways. This is the first reported study in mammals describing non-genetic, intergenerational transmission of metabolic sequelae of high fat diet from father to offspring. These findings support a role of fathers in metabolic programming of offspring and form a framework for further studies.

2014-01-20 | GSE33551 | GEO

Effects of dietary obesity in fathers on gene expression of islets in the female offspring (miRNA data)

Project description:The global prevalence of obesity is increasing across age and gender. The rising burden of obesity in young people contributes to the early emergence of type 2 diabetes. Having one parent obese is an independent risk factor for childhood obesity. While the detrimental impact of diet-induced maternal obesity on offspring is well established, the extent of the contribution of obese fathers is unclear, as is the role of non-genetic factors in the casual pathway. Here we show that paternal high fat diet exposure programmed β-cell ‘dysfunction’ in their F1 female offspring. Chronic high fat diet consumption in Sprague Dawley fathers led to increased body weight, adiposity, impaired glucose tolerance and insulin sensitivity. Relative to controls, their female offspring had lower body weight at day-1, increased pubertal growth rate, impaired insulin secretion and glucose tolerance, in the absence of obesity or increased adiposity. Paternal high fat diet altered the expression of 211 pancreatic islet genes in adult female offspring (P < 0.001); genes belonged to 8 functional clusters, including calcium ion binding, primary metabolic processes and ATP binding, and organ/system development. Broader KEGG pathway analysis of 2014 genes differentially expressed at the P < 0.01 level further demonstrated involvement of insulin and calcium signaling, and MAPK pathways. This is the first reported study in mammals describing non-genetic, intergenerational transmission of metabolic sequelae of high fat diet from father to offspring. These findings support a role of fathers in metabolic programming of offspring and form a framework for further studies.

2021-12-29 | GSE33563 | GEO

Single Cell RNA Sequencing reveals heterogenous tumor associated immune cell compartment in lean vs obese mice using an MC38 tumor model

Project description:Immunotherapy is life saving for some cancer patients and while obesity can promote cancer, it may also increase immunotherapy efficacy. Mechanisms of this effect have been unclear, although obesity can promote an inflammatory state that may modify tumor infiltrating lymphocytes and tumor associated macrophage (TAM) populations in tumors. To identify mechanisms by which obesity affects anti-tumor immunity, diet-induced obese and lean C57BL/6 mice received subcutaneous murine MC38-CEA1 colon cancer tumors. Obesity increased tumor growth rate and tumor burden. Fewer immune cells were present in tumors from obese mice, and the T cells had an activated and exhausted phenotype. Macrophages in obese animals had decreased expression of iNOS2 and MHCII, supporting a weaker “M1” anti-tumor phenotype compared to lean mice. When treated with anti-PD-1 antibodies, however, obese mice had a greater absolute decrease in tumor burden than lean mice. PD-1 blockade repolarized the macrophages to an M1-phentoype in obese mice, but this did not occur in the lean mice. Mechanistically, leptin is a pro-inflammatory adipokine that is increased in obesity and may mediate enhanced anti-tumor immunity in obesity. To test the effect of leptin on tumor growth and anti-tumor immunity, lean mice were treated with leptin and tumors were observed over time. Leptin had single-agent preventative and therapeutic anti-tumor efficacy similar to PD-1 checkpoint therapy. These data demonstrate that obesity has dual effects in cancer through promotion of tumor cell initiation while also enhancing anti-tumor immunity through elevated levels of leptin that can reprogram inflammatory macrophages.

2021-10-06 | GSE179936 | GEO

Targeting mitochondrial reactive oxygen species alleviates allergic airway disease in a mouse model of obese allergic asthma

Project description:Obesity is associated with severe, difficult to control asthma, and increased airway oxidative stress. Mitochondrial reactive oxygen species (mROS) are an important source of oxidative stress leading us to hypothesize that targeting mROS in obese allergic asthma might be an effective treatment strategy. Using a mouse model of house dust mite (HDM) induced allergic airway disease in mice fed a low- (LFD) or high-fat diet (HFD), and the mitochondrial antioxidant MitoQuinone (MitoQ); we investigated the effects of obesity and mROS on airway inflammation, remodelling and airway hyperreactivity (AHR). HDM induces airway inflammation, remodelling and hyperreactivity in both lean and obese mice. Obese allergic mice showed increased lung tissue eotaxin levels, airway tissue eosinophilia and AHR when compared to lean allergic mice. MitoQ reduced markers of airway inflammation, remodelling and hyperreactivity in both lean and obese allergic mice, and tissue eosinophilia in obeseHDM mice. mROS regulates cell signalling by protein oxidation of multiple downstream targets: MitoQ reduced HDM-induced cysteine-sulfenylation of several proteins including those involved in the unfolded protein response (UPR). In summary, mROS mediates the development of allergic airway disease and hence MitoQ might be effective for the treatment for asthma, and specific features of obese asthma.

2023-06-02 | PXD029715 | Pride

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