Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from mouse liver after chow and high-fat diet feeding

ABSTRACT: Epigenetic changes are present in multiple tissues of rodents and subjects suffering from obesity and type 2 diabetes. Especially, genes that are important for glucose and lipid metabolism seem to be at least co-regulated by DNA methylation. We aimed to investigate if altered DNA methylation in liver of mice can be induced by feeding a high-fat diet and if these changes can be reverted by weight loss. We used microarrays to measure the hepatic gene expression pattern in chow and high-fat diet (HFD) fed mice to identify dysregulated pathways which contribute to diet-induced obesity and insulin resistance. DNA methylation was measured of candidate genes to evaluate this as potential regulatory mechanism.

ORGANISM(S): Mus musculus

PROVIDER: GSE160646 | GEO | 2021/01/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Liver tissue HELP-tagging cytosine methylation data from C57BL/6J mice receiving high-fat diet with or without lingonberries

Project description:The C57BL/6J mouse model develops obesity and pre-diabetes when fed a high-fat diet. In this experiment, DNA methylation was assessed globally at specific CpG sites in liver tissue from mice receiving high-fat diet (45E% from fat) for 13 weeks (Control) or high-fat diet supplemented with 20% (w/w) of freeze-dried lingonberries (n=4). Our findings show that lingonberries prevent development of high-fat induced obesity, hepatic steatosis and low-grade inflammation, and the DNA was hypermethylated in mice receiving lingonberries compared to control. Genome wide hepatic DNA methylation comparison between mice fed high-fat diet with or without a lingonberry supplement (n=4/group).

2015-09-20 | E-GEOD-67277 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of Brown Adipose Tissues from 3bKO and fl/fl Control Mice after 20-week High-Fat Diet Feeding

Project description:A persistent influx of energy due to intake over expenditure leads to obesity. Increasing energy expenditure through activation of brown fat thermogenesis is a promising therapeutic strategy for the treatment of obesity. Epigenetic regulation has emerged as a key player in regulating brown fat development and thermogenic program. Here we aimed to study the role of DNA methyltransferase 3b (Dnmt3b), a DNA methyltransferase involved in de novo DNA methylation, in the regulation of brown fat function and energy homeostasis during diet-induced obesity (DIO). We have generated a genetic model with Dnmt3b deletion in brown fat-skeletal lineage precursor cells (3bKO mice) by crossing Dnmt3b-floxed (fl/fl) mice with Myf5-Cre mice. Female 3bKO mice were prone to diet-induced obesity and were insulin resistant. This was associated with decreased energy expenditure, which may largely account for the obese phenotype as there was no difference in food intake and locomotor activity between 3bKO and fl/fl mice. Dnmt3b deficiency impaired mitochondrial and thermogenic program in brown fat. Surprisingly, further RNA-seq analysis revealed a profound up-regulation of myogenic markers in the brown fat of 3bKO mice, suggesting a myocyte-like remodeling in brown fat, which may explain the impaired thermogenic program in brown fat. Further motif enrichment and pyrosequencing analysis suggested myocyte enhancer factor 2C (Mef2c) as a mediator for the myogenic alteration in Dnmt3b-deficient brown fat as indicated by decreased methylation at its promoter. Our data demonstrate that brown fat Dnmt3b is a key regulator of brown fat development, energy metabolism and obesity in female mice.

2021-12-01 | GSE173765 | GEO

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

Liver tissue HELP-tagging cytosine methylation data from C57BL/6J mice receiving high-fat diet with or without lingonberries

2015-09-20 | GSE67277 | GEO

Sodium ferrous citrate and 5-aminolevulinic acid improve type 2 diabetes by maintaining muscle and mitochondrial health

Project description:Objective Improving mitochondrial function is a promising strategy for intervention in type 2 diabetes mellitus. This study investigated the preventive effects of sodium ferrous citrate (SFC) and 5-aminolevulinic acid phosphate (ALA) on several metabolic dysfunctions associated with obesity because they have been shown to alleviate abnormal glucose metabolism in humans. Methods Six-week-old male C57BL/6J mice were fed with a normal diet, a high-fat diet, or a high-fat diet supplemented with SFC and ALA for 15 weeks. Results The simultaneous supplementation of SFC + ALA to high-fat diet-fed mice prevented loss of muscle mass, improved muscle strength, and reduced obesity and insulin resistance. SFC + ALA prevented abnormalities in mitochondrial morphology and reverted the diet effect on the skeletal muscle transcriptome, including the expression of glucose uptake and mitochondrial oxidative phosphorylation-related genes. In addition, SFC + ALA prevented the decline in mitochondrial DNA copy number by enhancing mitochondrial DNA maintenance and antioxidant transcription activity, both of which are impaired in high-fat diet-fed mice during long-term fasting. Conclusions These findings suggest that SFC + ALA supplementation exerts its preventive effects in type 2 diabetes mellitus via improved skeletal muscle and mitochondrial health, further validating its application as a promising strategy for the prevention of obesity-induced metabolic disorders.

2023-02-23 | GSE201092 | GEO

Obesity Remodels Activity and Transcriptional State of a Lateral Hypothalamic Brake on Feeding

Project description:We demonstrate that high fat diet (HFD)-induced obesity alters the transcriptional state of lateral hypothalamic glutamate neurons in mice.

2019-05-02 | GSE130597 | GEO

Time Restricted Feeding Mitigates Obesity Through Adipocyte Thermogenesis

Project description:In obesity, misalignment of feeding time with the light/dark environment results in disruption of peripheral circadian clocks. Conversely, restricting feeding to the active period mitigates metabolic syndrome through mechanisms that remain unknown. Here we show that adipocyte thermogenesis is essential for the healthful metabolic response to time restricted feeding. Genetic enhancement of adipocyte thermogenesis through ablation of Zfp423 attenuates obesity caused by circadian mistimed high fat diet feeding through a mechanism involving creatine metabolism. Circadian control of adipocyte creatine metabolism underlies timing of diet-induced thermogenesis, and enhancement of adipocyte circadian rhythms through overexpression of the clock activator Bmal1 ameliorates metabolic complications during diet induced obesity. These findings establish creatine mediated diet-induced thermogenesis as a bioenergetic mechanism driving metabolic benefits during time-restricted feeding.

2022-10-24 | GSE181443 | GEO

Folic acid supplementation alters the DNA methylation profile and improves insulin resistance in high-fat-diet-fed mice

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

Diet-Dependent Changes of the DNA Methylome Using a Göttingen Minipig Model for Obesity

Project description:In the present study, we have compared the promoter methylome in liver tissue of a Göttingen minipigs fed a high fat/fructose/cholesterol (FFC) diet with the promotor methylome of GM pigs fed the FFC diet and reverted to standard chow (FFC/SD), and fed standard chow (SD) respectively. Furthermore, we correlated the methylation patterns of key genes with their gene expression profiles in liver. We show that minipigs exhibited extensive, functionally relevant methylome perturbation under FFC diet compared to normal chow group. Also, the methylation levels were highly correlated with gene expression in key genes in the liver. Surprisingly, the diet-induced methylome variation could be only partially reversed to lean stage after replacing the FFC diet to normal chow diet, promotors of several obesity-related genes still remained differential methylated and expression was perturbed even after diet reversion.

2021-02-01 | GSE155197 | GEO

Expression data from murine colorectal tumors of mice fed a normal chow diet and a high fat diet

Project description:Obesity increases colorectal cancer despite other disturbances. We have used the AOM/DSS protocol to induce colitis-associated cancer in normal chow diet and high fat diet fed animals. Tumors were microdissected and global gene expression was analysed using microarray.

2019-01-16 | GSE113303 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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