E-MTAB-2569
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-2569 | ExpressionAtlas | 2015-07-13
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-2569-analysis-methods.tsv | Tabular | |||
| E-MTAB-2569-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-2569-configuration.xml | Xml | |||
| E-MTAB-2569-percentile-ranks.tsv | Tabular | |||
| E-MTAB-2569.condensed-sdrf.tsv | Tabular |
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Project description:The effect of high fat diet feeding on adipose tissue gene transcription regulation was investigated in C57Bl/6J mice using Affymetrix gene expression arrays. Expression profiling was determined in 5 months old male mice showing heterogeneous metabolic, hormonal and behavioral adaptation to high fat diet (40% fat) feeding for 15 weeks. Control mice were fed a standard carbohydrate chow. Six animals per group were used.
2014-04-13 | E-MTAB-2569 | biostudies-arrayexpress
Project description:We profiled the transcriptome of visceral adipose tissue from Foxp3.YFP-Cre Bmal1WT or Foxp3.YFP-Cre bmal1flox mice after 16 weeks of high-fat diet. We found that adipose tissue with Bmal1-deficient Tregs showed an increased enrichment of inflammatory pathways and a loss of metabolic pathways after high-fat diet feeding.
2022-07-28 | GSE206776 | GEO
Project description:Adipose tissue is a crucial metabolic organ maintaining energy homeostasis via catabolic and anabolic metabolism. As high-fat diet feeding leads to metabolic dysfunction, here, we aimed to study the effect of 8 weeks of high-fat diet feeding on WT mice and compare genes differentially regulated depending on the type of diets intaking.
2021-08-30 | GSE182930 | GEO
Project description:Age-related and/or high caloric intake driven changes in visceral adipose tissue contribute to the development of diabetes and cardiovascular disease. The lack of reliable, high-throughput methods to analyze the adipose tissue protein composition has limited our understanding of the protein networks responsible for metabolic regulation of various adipose depots. We have developed a proteomic approach using multiple-dimension liquid chromatography tandem mass spectrometry and multiplexed TMT labeling to analyze protein composition of epididymal adipose tissues isolated from mice fed either low or high fat diet for a short (8 weeks) or a long (18 weeks) term, and from mice that aged (26 weeks old) on low vs. high fat diets. Advancing age and high-fat diet feeding led to graded deterioration, with long-term high fat diet exposure being the worst of all measures of peripheral metabolic health such as body weight, adiposity, plasma fasting glucose, insulin, triglycerides, total cholesterol levels, and glucose and insulin tolerance tests. Epididymal adipose depot proteomic analysis identified >3300 proteins per sample. In response to short-term high fat diet, 43 proteins representing lipid metabolism (e.g., AACS, ACOX1, ACLY) and red-ox pathways (e.g., CPD2, CYP2E, SOD3) were significantly altered (FDR < 10%). Long-term high fat diet significantly altered 55 proteins associated with immune response (e.g., IGTB2, IFIT3, LGALS1) and rennin angiotensin system (e.g. ENPEP, CMA1, CPA3, ANPEP). Age-related changes on low fat diet significantly altered only 18 proteins representing mainly urea cycle (e.g., OTC, ARG1, CPS1), and amino acid biosynthesis (e.g., GMT, AKR1C6). Surprisingly, high fat diet driven age-related changes culminated with alterations in 155 proteins involving primarily the urea cycle (e.g., ARG1, CPS1), immune response/complement activation (e.g., C3, C4b, C8, C9, CFB, CFH, FGA), extracellular remodeling (e.g., EFEMP1, FBN1, FBN2, LTBP4, FERMT2, ECM1, EMILIN2, ITIH3) and apoptosis (e.g., YAP1, HIP1, NDRG1, PRKCD, MUL1) pathways. Our unbiased mass spectrometry method, tailored to adipose tissue, identified both age-related and high fat diet specific proteomic signatures. In addition to well-described immune and extracellular remodeling response to high fat feeding, we have uncovered the pronounced involvement of arginine metabolism in response to advancing age, and branched chain amino acid metabolism in early response to high fat feeding. We were able to uncouple age-related metabolic responses from those associated with caloric intake, a task otherwise difficult to achieve.
2017-03-27 | PXD005953 | Pride
Project description:Influenza A virus (IAV) infection-associated morbidity and mortality are a key global healthcare concern, necessitating the identification of novel therapies capable of reducing the severity of IAV infections. In this study, we show that the consumption of a low-carbohydrate, high-fat ketogenic diet (KD) protects mice from lethal IAV infection and disease. KD feeding resulted in an expansion of γδ T cells in the lung that improved barrier functions, thereby enhancing anti-viral resistance. Expansion of these protective γδ T cells required metabolic adaptation to a ketogenic diet, as neither feeding mice a high-fat high-carbohydrate diet nor providing chemical ketone body substrate that bypasses hepatic ketogenesis protected against infection. Therefore, KD mediated immune-metabolic integration represents a viable avenue towards preventing or alleviating influenza disease.
2019-08-29 | GSE136536 | GEO
Project description:Purpose: To study the effects of high-fat diet feeding in mouse liver tissues with and without the hepatocellular carcinoma-inducing carcinogen DEN. Here, we used RNA sequencing to identify gene expression patterns associated with high-fat diet feeding. Methods: C57BL/6N mice were injected at 2-weeks of age with vehicle control (PBS) or DEN. At 6 weeks, mice were randomized to control diet, or 60% high-fat diet. After 8-weeks of diet exposure, mice underwent a 13C6-glucose labelling protocol, and liver tissues were extracted for anlaysis (metabolomic, transcriptomic). RNA was isolated from mouse liver tissue using Triazol extraction, purified, and libraries generated using KAPA Stranded mRNA Sequencing kit. After cDNA synthesis, adapter ligation, and final cDNA library generation, samples were sequenced on a flow cell (1x50bp single-end reads) and HiSeq4000 (Illumina). Data processing was conducted in an NGS pipeline (Snakemake) and quality control was performed with FastQC. Trimmed data was analyzed for differential expression (DEseq2) and gene set enrichment analysis (GSEA) to look for KEGG pathways and gene ontologies (GO) of interest. Results: Using 13C6-glucose labelling, we determined there was a glycolytic phenotype caused by high-fat diet exposure. Therefore, we focused on a diet effect in our transcriptomcis dataset. By comparing control diet to high-fat diet liver tissue, we found gene sets invloved in peroxisomes and lipid metabolism to be enriched in high-fat diet exposed livers. These findings were in line with in vitro testing of a liver cell line, showing peroxisomal metabolism of palmitate drives ROS production and a glycolytic phenotype. Conclusions: We found high-fat diet exposed liver exhibits a strong metabolic phenotype towards increased glucose metabolism. At the transcriptome level, we found a lipid-reporgramming signature, and not a glucose metabolism signature. The lipid reprogramming signature was in line with in vitro work using liver cell lines, in which exposure to palmitate stimulated a glycolyitic phenotype that was inhibited by targeting peroxisomal-derived ROS species. In combination with metabolic and lipidomic data after long-term exposure to DEN and subsequent tumor formtion, we discovered that high-fat diet can prime liver tissue for carcinogenesis and tumor development by stimulating a Warburg-like metabolism. These findings suggest that fat can induce similar changes in non-transformed liver cells than found in HCC. In conclusion, we show that normal, non-transformed livers respond to fat by inducing glucose metabolism.
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Project description:Age-related and/or high caloric intake driven changes in visceral adipose tissue contribute to the development of diabetes and cardiovascular disease. The lack of reliable, high-throughput methods to analyze the adipose tissue protein composition has limited our understanding of the protein networks responsible for metabolic regulation of various adipose depots. We have developed a proteomic approach using multiple-dimension liquid chromatography tandem mass spectrometry and multiplexed TMT labeling to analyze protein composition of epididymal adipose tissues isolated from mice fed either low or high fat diet for a short (8 weeks) or a long (18 weeks) term, and from mice that aged (26 weeks old) on low vs. high fat diets. Advancing age and high-fat diet feeding led to graded deterioration, with long-term high fat diet exposure being the worst of all measures of peripheral metabolic health such as body weight, adiposity, plasma fasting glucose, insulin, triglycerides, total cholesterol levels, and glucose and insulin tolerance tests. Epididymal adipose depot proteomic analysis identified >3300 proteins per sample. In response to short-term high fat diet, 43 proteins representing lipid metabolism (e.g., AACS, ACOX1, ACLY) and red-ox pathways (e.g., CPD2, CYP2E, SOD3) were significantly altered (FDR < 10%). Long-term high fat diet significantly altered 55 proteins associated with immune response (e.g., IGTB2, IFIT3, LGALS1) and rennin angiotensin system (e.g. ENPEP, CMA1, CPA3, ANPEP). Age-related changes on low fat diet significantly altered only 18 proteins representing mainly urea cycle (e.g., OTC, ARG1, CPS1), and amino acid biosynthesis (e.g., GMT, AKR1C6). Surprisingly, high fat diet driven age-related changes culminated with alterations in 155 proteins involving primarily the urea cycle (e.g., ARG1, CPS1), immune response/complement activation (e.g., C3, C4b, C8, C9, CFB, CFH, FGA), extracellular remodeling (e.g., EFEMP1, FBN1, FBN2, LTBP4, FERMT2, ECM1, EMILIN2, ITIH3) and apoptosis (e.g., YAP1, HIP1, NDRG1, PRKCD, MUL1) pathways. Our unbiased mass spectrometry method, tailored to adipose tissue, identified both age-related and high fat diet specific proteomic signatures. In addition to well-described immune and extracellular remodeling response to high fat feeding, we have uncovered the pronounced involvement of arginine metabolism in response to advancing age, and branched chain amino acid metabolism in early response to high fat feeding. We were able to uncouple age-related metabolic responses from those associated with caloric intake, a task otherwise difficult to achieve.
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Project description:Nrg4 is a brown fat-enriched adipokine that binds to the liver and preserves metabolic homeostasis during chronic energy excess. Adipose tissue Nrg4 expression is reduced in mouse and human obesity. Nrg4 deficient mice develp more severe insulin resistance and hepatic fat accumulation upon high-fat diet feeding. We used microarrays to elucidate the metabolic pathways that are regulated by Nrg4 in the liver. Wild type and Neuregulin 4 (Nrg4) knockout mice were fed high-fat diet (Research Diets D12492) for eight weeks. Tissues were harvested under ad lib condition for RNA isolation and microarray hybridization using Affymetrix Mouse MG-430 PM Strip arrays. Three independent pools of WT and KO mouse liver RNA were included in the study. Manuscript title: A brown fat-enriched secreted factor preserves metabolic homeostasis through attenuating hepatic lipogenesis, (journal information TBD)
2014-11-17 | E-GEOD-53877 | biostudies-arrayexpress