Effect of high fat diet feeding on adipose tissue macrophages
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA706728 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13859521.fastq.gz | Fastqsanger.gz | |||
| SRR13859522.fastq.gz | Fastqsanger.gz |
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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:The adipose tissue plays an important role in controlling whole-body energy balance, and proper regulation of adipose tissue function is essential for metabolic health. In response to energy surplus, the adipose tissue needs to expand, which may lead to local areas of hypoxia within the tissue. This is thought to promote whole-body insulin resistance. Here we report that DICER, a key enzyme in the maturation of miRNAs and a potential marker of adipocyte health, is profoundly downregulated in mouse adipose tissue within the first week of high-fat diet (HFD) feeding, and this effect is sustained in response to long-term HFD feeding. The downregulation of DICER protein occurs in both mature adipocytes and in the stromal vascular cells. Mechanistically, we provide evidence that hypoxia and hypoxia-inducible factor 1-α (HIF1α) facilitate ubiquitination of DICER to target it for autophagy-mediated degradation, and we show that DICER and HIF1α interact in adipose tissue after HFD feeding, which may signal for DICER degradation. Finally, despite reductions in DICER protein, we were not able to detect any differences in global miRNA levels in subcutaneous adipose tissue of mice after one or three weeks of HFD-feeding. In conclusion, the nutritional challenge of HFD feeding in mice leads to a large reduction in adipose tissue DICER protein, which is induced by hypoxia during tissue expansion and mediated through an interaction with HIF1α.
2024-11-12 | GSE254511 | GEO
Project description:The objective of the experiment was to dissect the effects of a high-fat diet on juvenile adipose tissue gene expression under conditions of excess calorie intake versus normal calorie intake in comparison to a standard low-fat diet. For this purpose juvenile mice were fed (A) a standard low-fat diet (CD), (B) a high-fat diet ad libitum (excess calorie intake) (HFD) and (C) a high-fat diet with calorie consumption restricted to the calorie consumption of the CD diet (R-HFD). RNA expression was profiled after 1 week of feeding in the periuterine fat depot.
2019-04-09 | E-MTAB-7755 | biostudies-arrayexpress
Project description:Analysis of gene expression in adipose tissue of female mice after continuous high fat diet (HFD) feeding for three generations. The hypothesis in this study is that continuous HFD feeding has transgenerational amplification effects to the offspring. Results provide important information on the impacts of over-nutrition over one generation on the offspring, such as transgenerational up-regulated or down-regulated genes. Total RNA was obtained from adipose tissue of the HFD fed mice, including F0, F1 and F2 generations. Normal chow fed mice were used as controls.
2013-05-10 | E-GEOD-37238 | biostudies-arrayexpress
Project description:Analysis of gene expression in adipose tissue of female mice after continuous high fat diet (HFD) feeding for three generations. The hypothesis in this study is that continuous HFD feeding has transgenerational amplification effects to the offspring. Results provide important information on the impacts of over-nutrition over one generation on the offspring, such as transgenerational up-regulated or down-regulated genes.
2013-05-10 | GSE37238 | 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: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:DICER is downregulated in mouse adipose tissue during high-fat diet feeding
| PRJNA1070687 | ENA
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.
2018-07-03 | MSV000082569 | MassIVE
Project description:Despite wide efforts in the last decade, signaling aberrations associated with obesity remain enigmatic. Here, we carried out phosphoproteomic analysis of mouse white adipose tissues (WAT) upon low-fat diet (LFD) and high-fat diet (HFD) to dissect underlying molecular mechanisms of obesity. Of the 7696 phosphopeptides quantified, 191 proteins including various insulin-responsive proteins and metabolic enzymes functioning in lipid homeostasis, exhibited differential phosphorylation with high-fat feeding. Kinase predictions and integrated network analysis identified several deregulated kinase signaling pathways, and suggested possibilities of HFD-induced transcriptional rewiring. Further, functional validation of a novel HFD-responsive site on cytoplasmic acetyl-coA forming ACSS2 (S263) suggested that the phosphorylation is important in regulating insulin signaling and maintaining triglyceride levels. This study represents one of the first comprehensive phosphoproteome data in mouse obesity models, and describes a systems-level approach for identifying deregulated molecular events and potential therapeutic targets in the context of high-fat feeding and adipocyte perturbation.
2016-05-20 | PXD002927 | Pride