Ontology highlight
ABSTRACT:
PROVIDER: PRJNA551310 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11942957_1.fastq.gz | Fastqsanger.gz | |||
| SRR11942957_2.fastq.gz | Fastqsanger.gz | |||
| SRR11942958_1.fastq.gz | Fastqsanger.gz | |||
| SRR11942958_2.fastq.gz | Fastqsanger.gz | |||
| SRR11942959_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 40 |
Similar Datasets
Project description:Microbiome changes after geranylgeraniol supplementation in high-fat diet-induced obese mice
| PRJNA637806 | ENA
Project description:Folic acid (FA) supplementation may protect from obesity and insulin resistance, the effects and mechanism of FA on chronic high-fat-diet-induced obesity-related metabolic disorders are not well elucidated. We adopted a genome-wide approach to directly examine whether FA supplementation affects the DNA methylation profile of mouse adipose tissue and identify the functional consequences of these changes. Mice were fed a high-fat diet (HFD), normal diet (ND) or an HFD supplemented with folic acid (20 μg/ml in drinking water) for 10 weeks, epididymal fat was harvested, and genome-wide DNA methylation analyses were performed using methylated DNA immunoprecipitation sequencing (MeDIP-seq). Mice exposed to the HFD expanded their adipose mass, which was accompanied by a significant increase in circulating glucose and insulin levels. FA supplementation reduced the fat mass and serum glucose levels and improved insulin resistance in HFD-fed mice. MeDIP-seq revealed distribution of differentially methylated regions (DMRs) throughout the adipocyte genome, with more hypermethylated regions in HFD mice. Methylome profiling identified DMRs associated with 3787 annotated genes from HFD mice in response to FA supplementation. Pathway analyses showed novel DNA methylation changes in adipose genes associated with insulin secretion, pancreatic secretion and type 2 diabetes. The differential DNA methylation corresponded to changes in the adipose tissue gene expression of Adcy3 and Rapgef4 in mice exposed to a diet containing FA. FA supplementation improved insulin resistance, decreased the fat mass, and induced DNA methylation and gene expression changes in genes associated with obesity and insulin secretion in obese mice fed a HFD.
2018-06-30 | GSE97576 | GEO
Project description:We reported the gene expression profiles of prostate dorsal-lateral-ventral glands of prostate-specific Pten-/- mice on AIN93M diet, 60%Kcal high-fat diet, and AIN93M diet containing 0.05% delta-tocotrienol at 20 weeks of age.
2021-09-10 | GSE182980 | GEO
Project description:We investigated the plasma and liver proteome changes in liver fibrosis in mice induced by hepatocyte-specific knockout of nicotinamide phosphoribosyltransferase (Nampt) upon a low-methionine, choline-free 60% high-fat (MCD) diet at multiple time points. We also investigated whether supplementation with nicotinamide riboside could alleviate liver injury and how the liver proteome changes upon NR supplementation.
2021-11-04 | PXD017170 | Pride
Project description:Although aging is a physiological process to which all organisms are subject, the presence of obesity and type 2 diabetes accelerates biological aging. Recent studies have demonstrated the causal relationships between dietary interventions suppressing obesity and type 2 diabetes and delaying the onset of age-related endocrine changes. Curcumin, a natural antioxidant, has putative therapeutic properties such as reinstating insulin sensitivity in obese mice. However, how curcumin contributes to maintaining insulin homeostasis in aged organisms largely remains unclear. Thus, the objective of this study is to examine the pleiotropic effect of dietary curcumin on insulin homeostasis in a diet-induced obese (DIO) aged mouse model. Aged (18-20 months old) male mice given a high-fat high-sugar diet supplemented with curcumin displayed a different metabolic phenotype compared to mice given a high-fat high-sugar diet alone. Furthermore, curcumin supplementation altered hepatic gene expression profiling, especially insulin signaling and senescence pathways. We then mechanistically investigated how curcumin functions to fine-tune insulin sensitivity. We found that curcumin supplementation increased hepatic insulin degrading enzyme (IDE) expression levels and preserved islet integrity, both of which are beneficial during aging. Our findings suggest that the multifaceted therapeutic potential of curcumin can be used as a protective agent for age-induced metabolic diseases.
2021-11-04 | GSE186971 | GEO
Project description:We used Affymetrix microarrays to investigate gene expression changes in the liver of wild-type C57BL-6 mice exposed to a high-fat diet that might have been caused by the oral consumption of the probiotic B. pseudocatenulatum CECT 7765. The aim of this work was to determine whether the daily intake (by oral gavage) of the probiotic (P) B. pseudocatenulatum for seven weeks exerted any modulatory effects, at the level of gene expression, in the liver of C57BL-6 male mice exposed to a high-fat diet (HFD). Male mice were randomly assigned to four experimental groups (n= 5 animals per group) as follows: (1) control group, fed a standard diet (SD); (2) obese group, fed a high-fat diet (HFD); (3) a group that received the SD and a daily dose of the probiotic (1M-CM-^W109 CFU B. pseudocatenulatum CECT 7765) (SD+P); and (d) an obese group that was fed the HFD and a daily dose of the probiotic (1M-CM-^W109 CFU B. pseudocatenulatum CECT 7765) (HFD+P). At the end of the experimental procedure total RNA was extracted from the liver to compare differential gene expression between the groups. Liver differential gene expression after 7 weeks of supplementation between: 1) the HFD group and the SD group (effects of the high-fat diet); 2) the HFD+P and the HFD (effects of the probiotic on the consumption of a high-fat diet) and 3) the SD+P group and the SD (direct effects of the probiotic on the liver of animals consuming a normal diet).
2012-11-20 | E-GEOD-40638 | 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