Diet-induced chromatin remodeling in mice livers
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE55581 | GEO | 2014/07/17
SECONDARY ACCESSION(S): PRJNA240124
REPOSITORIES: GEO
Similar Datasets
Project description:The tissue-specific packaging of the genome into the nucleus through chromatin is fundamentally involved in gene regulation, and aberrant modifications to chromatin are a hallmark of many diseases. We show here that a high fat (HF) diet leads to substantial chromatin remodeling in the livers of C57BL/6J mice, as compared to mice fed a control diet. Regions of the genome that display the greatest variation in chromatin accessibility between HF and control regions are targeted by transcription factors with known roles in the liver including HNF4α, CEBP/α, and FOXA1. Whereas livers of DBA/2J mice fed a HF or control diet also demonstrate diet-induced chromatin remodeling, the regions displaying the greatest variation are largely distinct from those observed in B6 livers, indicating a crosstalk between genetic and epigenetic components in determining how diet-induced chromatin remodeling is associated with metabolic disease progression. Examination of chromatin remodeling with FAIRE-seq in livers of mice (C57BL/6J and DBA/2J) fed a high fat or control diet. Complemented with gene expression and H3K4me1 analyses
2014-07-17 | E-GEOD-55581 | biostudies-arrayexpress
Project description:Obesity is a highly heritable complex disease that results from the interaction of multiple genetic and environmental factors. Formerly obese individuals are susceptible to metabolic disorders later in life, even after lifestyle changes are made to mitigate the obese state. This is reminiscent of the metabolic memory phenomenon originally observed for persistent complications in diabetic patients, despite subsequent glycemic control. Epigenetic modifications represent a potential mediator of this observed memory. We previously demonstrated that a high fat (HF) diet leads to changes in chromatin accessibility in the mouse liver. The regions of greatest chromatin changes in accessibility are largely strain dependent, indicating a genetic component in diet-induced chromatin alterations. We have now examined the persistence of diet-induced chromatin accessibility changes upon diet reversal in two strains of mice. We find that a substantial fraction of loci that undergo chromatin accessibility changes with HF diet remain in the remodeled state after diet reversal in C57BL/6J mice. In contrast, the vast majority of diet-induced chromatin accessibility changes in A/J mice are transient. Our data also indicate that the persistent chromatin accessibility changes observed in C57BL/6J are associated with specific transcription factors and histone posttranslational modifications. The persistent loci identified here are likely to be contributing to the overall phenotype and are attractive targets for therapeutic intervention. Examination of chromatin remodeling with FAIRE-seq in livers of C57BL/6J and A/J mice on three diet regimen: 1) control diet for 16 weeks, 2) high fat diet for 16 weeks, or 3) high fat diet for 8 weeks with control diet for 8 weeks. These chromatin profiles were complemented with gene expression data (RNA-seq)
2016-03-22 | E-GEOD-75984 | biostudies-arrayexpress
Project description:Both exposure to ionizing radiation and obesity have been associated with various pathologies including cancer. There is a crucial need in better understanding the interactions between ionizing radiation effects (especially at low doses) and other risk factors, such as obesity. In order to evaluate radiation responses in obese animals, C3H and C57BL/6 mice fed a control low fat or a high fat (HF) diet were exposed to fractionated doses of X-rays (4×0.75 Gy). Bone marrow micronucleus assays did not suggest a modulation of radiation-induced genotoxicity by HF diet. Both HF diet and irradiation resulted in increased oxidative damage, H2AX levels and proliferation in C57BL/6 mouse liver. Using methylation-specific PCR, we observed that the promoters of p16 and Dapk genes were methylated in the livers of C57BL/6 mice fed a HF diet (irradiated and non-irradiated); Mgmt promoter was methylated in irradiated and/or HF diet-fed mice. In addition, methylation PCR arrays identified Ep300 and Socs1 (whose promoters exhibited higher methylation levels in non-irradiated HF diet-fed mice) as potential targets for further studies. We then compared microRNA regulations after radiation exposure in the livers of C57BL/6 mice fed a normal or an HF diet, using microRNA arrays. Interestingly, radiation-triggered microRNA regulations observed in normal mice were not observed in obese mice. All together, our results suggested the existence of dietary effects on radiation responses (especially epigenetic regulations) in mice, possibly in relationship with obesity-induced chronic oxidative stress. C57BL/6J mice were fed a normal or a high-fat diet and exposed to 4 x 0.75 Gy X-rays. miRNA expression was measured in the livers of 3 mice for each experimental group.
2013-11-09 | E-GEOD-47956 | biostudies-arrayexpress
Project description:Chromatin accessibility is a hallmark of active regulatory function in the genome and variation of chromatin accessibility across individuals has been shown to contribute to complex traits and disease susceptibility. However, the mechanisms responsible for chromatin variation among different individuals and how this variation contributes to phenotypic diversity remain poorly understood. We examined chromatin accessibility variation in liver tissue from seven strains of adult mice that have phenotypic diversity in response to a high-fat/high-sucrose diet. Remarkably, nearly 40% of the loci with the greatest degree of chromatin variability across the strains are associated with transposable elements (TEs), with evolutionarily younger TEs being particularly enriched for regions of chromatin variation. We found that evolutionary younger and older TEs have differential chromatin accessibility profiles and are enriched for binding sites of different transcription factors, indicating the role of TEs in the evolution of regulatory networks in the liver. We also demonstrate that TE polymorphisms and epigenetic regulation of TEs contribute to regulatory variation across different strains through providing binding sites for liver transcription factors. Intriguingly, variable chromatin loci that are associated with liver metabolism are primarily TE-associated. We demonstrate that TEs contribute to regulatory variation in liver and have downstream effects on metabolism. Our data reveal TEs as a novel and important contributor to regulatory and phenotypic variation in the liver and suggest that regulatory variation at TEs is a major contributor to phenotypic variation in populations. Examination of chromatin accessibility with FAIRE-seq in livers of male mice (A/J, AKR/J, BALB/cJ, C57BL/6J, C3H/HeJ, CBA/J, DBA/2J, BXH2/TyJ, and BXH19/TyJ) fed a high-fat, high-sucrose diet.
2016-07-14 | E-GEOD-75770 | biostudies-arrayexpress
Project description:Both exposure to ionizing radiation and obesity have been associated with various pathologies including cancer. There is a crucial need in better understanding the interactions between ionizing radiation effects (especially at low doses) and other risk factors, such as obesity. In order to evaluate radiation responses in obese animals, C3H and C57BL/6 mice fed a control low fat or a high fat (HF) diet were exposed to fractionated doses of X-rays (4×0.75 Gy). Bone marrow micronucleus assays did not suggest a modulation of radiation-induced genotoxicity by HF diet. Both HF diet and irradiation resulted in increased oxidative damage, H2AX levels and proliferation in C57BL/6 mouse liver. Using methylation-specific PCR, we observed that the promoters of p16 and Dapk genes were methylated in the livers of C57BL/6 mice fed a HF diet (irradiated and non-irradiated); Mgmt promoter was methylated in irradiated and/or HF diet-fed mice. In addition, methylation PCR arrays identified Ep300 and Socs1 (whose promoters exhibited higher methylation levels in non-irradiated HF diet-fed mice) as potential targets for further studies. We then compared microRNA regulations after radiation exposure in the livers of C57BL/6 mice fed a normal or an HF diet, using microRNA arrays. Interestingly, radiation-triggered microRNA regulations observed in normal mice were not observed in obese mice. All together, our results suggested the existence of dietary effects on radiation responses (especially epigenetic regulations) in mice, possibly in relationship with obesity-induced chronic oxidative stress.
2013-11-09 | GSE47956 | GEO
Project description:High fat diet (HF) rodent models have contributed significantly to the dissection of the pathophysiology of the insulin resistance syndrome, but their phenotype varies distinctly between different studies. Here, we have analyzed gene expression patterns in livers of animals fed with different HF with varying fatty acid compositions. Keywords: diet-gene interaction
2005-10-28 | GSE3512 | GEO
Project description:Diet-induced chromatin remodeling in mice livers
| PRJNA240124 | ENA
Project description:High fat diet (HF) rodent models have contributed significantly to the dissection of the pathophysiology of the insulin resistance syndrome, but their phenotype varies distinctly between different studies. Here, we have analyzed gene expression patterns in livers of animals fed with different HF with varying fatty acid compositions. Experiment Overall Design: Male Wistar rats were fed with high fat diets (42 energy%, fat sources: lard, olive oil; coconut fat; cod liver oil). Weight, food intake, whole body insulin tolerance and plasma parameters of glucose and lipid metabolism were measured during a 12 week diet course. Liver histologies and hepatic gene expression profiles using AffymetrixR gene chips were obtained.
2007-10-10 | E-GEOD-3512 | biostudies-arrayexpress
Project description:The present study was conducted to evaluate the effects of the intake of three types of coffee (caffeinated, decaffeinated, and green unroasted coffee) on the livers of C57BL/6J mice fed a high-fat diet, and to extensively elucidate the physiological responses to coffee intake by analysing the findings obtained from a comprehensive transcriptomic analysis using DNA microarrays. The present study was conducted to evaluate the effects of the intake of three types of coffee (caffeinated, decaffeinated, and green unroasted coffee) on the livers of C57BL/6J mice fed a high-fat diet, and to extensively elucidate the physiological responses to coffee intake by analysing the findings obtained from a comprehensive transcriptomic analysis using DNA microarrays. Briefly, 7-week-old male C57BL/6J mice purchased from Charles River Laboratories Japan (Yokohama) were divided into the following five groups. The normal diet group (ND group) was fed D12450B (10 kcal% fat, Research Diets, New Brunswick, NJ, USA). The high-fat diet group (HF group) was fed D12492 (60 kcal% fat, Research Diets, New Brunswick, NJ, USA). The caffeinated coffee group (HFCC group) was fed a high-fat diet containing 2% caffeinated freeze-dried coffee. The decaffeinated coffee group (HFDC group) was fed a high-fat diet containing 2% decaffeinated freeze-dried coffee. The green unroasted coffee group (HFGC group) was fed a high-fat diet containing 2% unroasted caffeinated freeze-dried coffee. The mice had ad libitum access to their diets and drinking water. After 9 weeks, mice were sacrificed and the livers were subjected to the Affymrtix DNA microarray experiment.
2013-12-10 | E-GEOD-53131 | biostudies-arrayexpress
Project description:Obesity is a highly heritable complex disease that results from the interaction of multiple genetic and environmental factors. Formerly obese individuals are susceptible to metabolic disorders later in life, even after lifestyle changes are made to mitigate the obese state. This is reminiscent of the metabolic memory phenomenon originally observed for persistent complications in diabetic patients, despite subsequent glycemic control. Epigenetic modifications represent a potential mediator of this observed memory. We previously demonstrated that a high fat (HF) diet leads to changes in chromatin accessibility in the mouse liver. The regions of greatest chromatin changes in accessibility are largely strain dependent, indicating a genetic component in diet-induced chromatin alterations. We have now examined the persistence of diet-induced chromatin accessibility changes upon diet reversal in two strains of mice. We find that a substantial fraction of loci that undergo chromatin accessibility changes with HF diet remain in the remodeled state after diet reversal in C57BL/6J mice. In contrast, the vast majority of diet-induced chromatin accessibility changes in A/J mice are transient. Our data also indicate that the persistent chromatin accessibility changes observed in C57BL/6J are associated with specific transcription factors and histone posttranslational modifications. The persistent loci identified here are likely to be contributing to the overall phenotype and are attractive targets for therapeutic intervention.
2016-03-22 | GSE75984 | GEO