Gene expression in the liver and colon of mice fed diets HH, LL, HL and LH
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE68179 | GEO | 2015/04/23
SECONDARY ACCESSION(S): PRJNA281956
REPOSITORIES: GEO
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Project description:Transcriptional profiling of mice fed a diet deficient in selenium and folate during weaning and in utero (LL), a diet deficient in selenium and folate during weaning but not in utero (HL), a diet sufficient in selenium and folate during weaning but deficient in utero (LH), and a diet sufficient in selenium and folate during weaning and in utero (HH) 2 colour microarray, reference design. Biological replicates: 6 per treatment group. The reference RNA was extracted from a whole pregnant C57 mouse and foetus. The whole body was homogenised and RNA was extracted using an AllPrep(r) DNA/RNA/Protein mini kit (Qiagen, Cat number 80004).
2015-04-23 | E-GEOD-68179 | biostudies-arrayexpress
Project description:Background: Consumption of high fat diets has negative impacts on health and well-being, some of which may be epigenetically regulated. Selenium and folate are two compounds which influence epigenetic mechanisms. We investigated the hypothesis that post-weaning supplementation with adequate levels of selenium and folate in mouse offspring fed a high fat, low selenium and folate diet during gestation and lactation will lead to epigenetic changes of potential importance for long-term health. Female offspring of mothers fed the experimental diet were either maintained on this diet (HF-low-low), or weaned onto a high-fat diet with sufficient levels of selenium and folate (HF-low-suf), for 8 weeks. Gene and protein expression, DNA methylation, and histone modifications were measured in colon and liver of female offspring. Results: Adequate levels of selenium and folate post-weaning affected gene expression in colon and liver of offspring, including decreasing Slc2a4 gene expression. Protein expression was only altered in the liver. There was no effect of adequate levels of selenium and folate on global histone modifications in the liver. Global liver DNA methylation was decreased in mice switched to adequate levels of selenium and folate, but there was no effect on methylation of specific CpG sites within the Slc2a4 gene in liver. Conclusions: Post-weaning supplementation with adequate levels of selenium and folate in female offspring of mice fed high-fat diets during gestation and lactation can alter global DNA methylation in liver. This may be one mechanism by which the negative effects of a poor diet during early life can be ameliorated. Further research is required to establish what role epigenetic changes play in mediating observed changes in gene and protein expression, and the relevance of these changes to health.
2013-06-01 | GSE43038 | GEO
Project description:Background: Consumption of high fat diets has negative impacts on health and well-being, some of which may be epigenetically regulated. Selenium and folate are two compounds which influence epigenetic mechanisms. We investigated the hypothesis that post-weaning supplementation with adequate levels of selenium and folate in mouse offspring fed a high fat, low selenium and folate diet during gestation and lactation will lead to epigenetic changes of potential importance for long-term health. Female offspring of mothers fed the experimental diet were either maintained on this diet (HF-low-low), or weaned onto a high-fat diet with sufficient levels of selenium and folate (HF-low-suf), for 8 weeks. Gene and protein expression, DNA methylation, and histone modifications were measured in colon and liver of female offspring. Results: Adequate levels of selenium and folate post-weaning affected gene expression in colon and liver of offspring, including decreasing Slc2a4 gene expression. Protein expression was only altered in the liver. There was no effect of adequate levels of selenium and folate on global histone modifications in the liver. Global liver DNA methylation was decreased in mice switched to adequate levels of selenium and folate, but there was no effect on methylation of specific CpG sites within the Slc2a4 gene in liver. Conclusions: Post-weaning supplementation with adequate levels of selenium and folate in female offspring of mice fed high-fat diets during gestation and lactation can alter global DNA methylation in liver. This may be one mechanism by which the negative effects of a poor diet during early life can be ameliorated. Further research is required to establish what role epigenetic changes play in mediating observed changes in gene and protein expression, and the relevance of these changes to health. Female wild type C57BL/6 mice (Animal Resource Centre, Western Australia) were fed a High Fat diet containing low levels of selenium and folate (HF-Low) for 7 days prior to mating with male C57BL/6 mice (Ruakura Small Animal Facility, Hamilton, New Zealand). Mothers were maintained on the HF-Low diet throughout gestation and lactation. Offspring of these female mice were randomly assigned to one of two different dietary treatments: either the same diet as the mothers (HF-Low), or a High Fat diet containing adequate selenium and folate (HF-Suf). At 12 weeks of age, mice were euthanized and colon and liver samples taken for microarray, proteomics, and DNA methylation analyses. Genomic DNA, total RNA and protein from whole colon and liver tissue was extracted using an AllPrepM-BM-. DNA/RNA/Protein mini kit (Qiagen, Cat number 80004). Colon and liver RNA from six female offspring on the HF-Low diet was compared with colon and liver RNA from six female offspring on the HF-Suf diet. All individual RNA samples were hybridized against a common reference RNA on separate arrays. The reference RNA was prepared by pooling in equimolar proportions RNA extracted from the intestine and liver of twelve female C57BL/6 mice, these being all of the mice from which samples were derived for microarray analysis in the current study.
2013-06-01 | E-GEOD-43038 | biostudies-arrayexpress
Project description:Scope: The âPredictive Adaptive Responseâ hypothesis suggests the in utero environment when mismatched with the post-natal environment can influence later life health. Underlying mechanisms are poorly understood, but may involve gene transcription changes, regulated via epigenetic mechanisms. Methods and Results: In a 2x2 factorial design, female C57Bl/6 mice were randomised to low or normal folate diets (0.4mg/ or 2mg folic acid/kg diet) prior to and during pregnancy and lactation with. At weaning, offspring were randomised to high or low fat diets at weaning. Genome-wide gene expression and promoter DNA methylation were measured using microarrays in adult male livers. Maternal folate depletion and high fat intake post-weaning influenced gene expression (1959 and 1612 genes respectively) and promoter DNA methylation (208 and 344 loci respectively) but changes in expression and methylation were poorly matched for both dietary interventions. Expression of 667 genes was altered in response to both maternal folate depletion and post-weaning high fat feeding. In addition, there was evidence that the combined dietary insult (i.e. maternal folate depletion followed by high fat post-weaning) exerted the largest expression change for most of these genes. Conclusion: Our observations align with, and provide evidence in support of a potential underlying mechanism for, the âPredictive Adaptive Responseâ hypothesis. Elucidation of these mechanisms may identify targets for interventions to mitigate effects of adverse nutrition exposures during early development on disease risk in later life.
2017-05-22 | E-MTAB-4987 | biostudies-arrayexpress
Project description:We hypothesized that the availability of folate, a soluble B vitamin, would alter the levels of DNA methylation in spermatogenesis with consequences for the sperm epigenome and pregnancy outcomes. We fed male mice with either a folate-deficient or a folate-sufficient diet throughout life. Males fed the folate-deficient diet had offspring with increased birth defects, which included craniofacial and musculoskeletal malformations. These phenotypes corresponded to developmental genes with altered methylation in sperm. To determine if there was transmission of epigenetic effects from sires to offspring, global gene expression levels were assessed in placenta from 18.5 dpc fetuses sired by either a folate-sufficient or folate-deficient male. Gene expression was measured in placenta of 18.5 dpc fetuses sired by either a folate sufficient male (n=4 placentas from different litters and different fathers) or a folate deficient (FD) male (n=4 placentas from different litters and different fathers).
2013-11-06 | E-GEOD-51819 | biostudies-arrayexpress
Project description:Abstract Scope: The âPredictive Adaptive Responseâ hypothesis suggests the in utero environment when mismatched with the post-natal environment can influence later life health. Underlying mechanisms are poorly understood, but may involve gene transcription changes, regulated via epigenetic mechanisms. Methods and Results: In a 2x2 factorial design, female C57Bl/6 mice were randomised to low or normal folate diets (0.4mg/2mg folic acid/kg diet) prior to and during pregnancy and lactation with, offspring randomised to high or low fat diets at weaning. Genome-wide gene expression and promoter DNA methylation were measured using microarrays in adult male livers. Maternal folate depletion and high fat intake post-weaning influenced gene expression (1959 and 1612 genes respectively) and promoter DNA methylation (208 and 344 loci respectively) but changes in expression and methylation were poorly matched for both dietary interventions. Expression of 667 genes was altered in response to both maternal folate depletion and post-weaning high fat feeding. In addition, there was evidence that the combined dietary insult (i.e. maternal folate depletion followed by high fat post-weaning) exerted the largest expression change for most of these genes. Conclusion: Our observations align with, and provide evidence in support of a potential underlying mechanism for, the âPredictive Adaptive Responseâ hypothesis. Elucidation of these mechanisms may identify targets for interventions to mitigate effects of adverse nutrition exposures during early development on disease risk in later life.
2017-05-22 | E-MTAB-4990 | biostudies-arrayexpress
Project description:ChIP-Sequencing for H3K4me3 was performed on the sperm of individual mice fed a folate sufficient or folate deficient diet, and on a wildtype or KDM1A overexpressing transgenic background. Ultra-Low-Input ChIP-Sequencing was performed on 8-cell embryos from male wildtype mice fed a folate sufficient or folate deficient diet. We identified regions of the sperm epigenome that were sensitive to a folate deficient diet and found that multiple epigenetic stressors could cumulatively alter H3K4me3 in sperm. Additionally, we found that alterations in H3K4me3 levels in the sperm of folate deficient males were retained in the pre-implantation embryo. Finally, low-input RNA-Seq on 8-cell embryos from folate sufficient or folate deficient males on a wildtype or KDM1A transgenic background allowed us identify transcripts with deregulated gene expression in the pre-implantation embryo. Regulating promoters with aberrant transcription in the 8-cell embryos overlapped promoters with altered H3K4me3 in sperm.
2021-02-18 | GSE135678 | GEO
Project description:We hypothesized that the availability of folate, a soluble B vitamin, would alter the levels of DNA methylation in spermatogenesis with consequences for the sperm epigenome and pregnancy outcomes. We fed male mice with either a folate-deficient or a folate-sufficient diet throughout life. Males fed the folate-deficient diet had offspring with increased birth defects, which included craniofacial and musculoskeletal malformations. These phenotypes corresponded to developmental genes with altered methylation in sperm. To determine if there was transmission of epigenetic effects from sires to offspring, global gene expression levels were assessed in placenta from 18.5 dpc fetuses sired by either a folate-sufficient or folate-deficient male.
2013-11-06 | GSE51819 | GEO
Project description:Initiation of a vitamin A deficient diet in mid-gestation, maintained in the post-weaning diet is sufficient to cause liver and serum retinoid depletion. Wild type C57Bl/6J timed mated pregnant dams were administered either a defined vitamin A sufficient low fat (12 percent kcal from fat) diet or matched vitamin A deficient diet from embryonic day 10.5. Vitamin A sufficient offspring were weaned onto either a high fat diet (60 percent kcal from fat) or maintained on the low fat 12 percent kcal from fat diet for 11 weeks (14 weeks of age). Gestational vitamin A deficient offspring were maintained on the same vitamin A deficient diet until 14 weeks of age. The impact of the maternal diet on a post-weaning high fat diet was compared to a standard maternal breeder diet followed by the post-weaning high fat diet.
2016-10-12 | GSE87845 | GEO
Project description:Previous studies in our laboratory have shown that low folate diet (control diet with 2mg folate/kg, low folate diet with 0.3mg folate/kg) can induce intestinal tumors in BALB/c mice. We used microarrays to compare MTHFR+/+ BALB/c mice fed control diet and MTHFR+/- BALB/c mice fed low folate diet. After weaning, 4 BALB/c Mthfr +/+ mice were fed with a control diet (CD, 2mg folate/kg) and 4 BALB/c Mthfr +/- mice were fed a low folate diet (FD, 0.3mg folate/kg) for 1 year. Both diets contain succinylsulfanthiozole (1%) to prevent folate synthesis by intestine microbial biota.
2013-12-03 | E-GEOD-34011 | biostudies-arrayexpress