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Global chromatin accessibility using an Assay for Transposase-Accessible Chromatin sequencing (ATAC-seq) reveals epigenomic reprogramming of Adipose tissue macrophages toward proinflammatory and proangiogenic phenotypes in formerly obese mice.

ABSTRACT: We report sustained changes in the chromatin accessibility landscape of adipose tissue macrophages (ATMs) from high fat diet (HFD)-fed mice persist long after return to regular diet (RD). We compared the data of ATAC-seq performed on nuclei extracted from FACS-sorted ATMs isolated from HFD, RD-RD and HFD-RD-fed mice. Inter-group comparisons revealed the highest diversity and hence the greatest number of differentially accessible regions (DARs) to occur between ATMs from RD-RD and HFD-RD-fed mice, and considerably fewer DARs were identified between ATMs from HFD-RD vs HFD-fed mice. Association of DARs with the nearest gene and gene ontology (GO) enrichment analysis revealed considerable pathway enrichment, especially pathways coding for angiogenesis and inflammatory response, in HFD-RD group when compared to RD-RD group. The results altogether indicated that most changes in chromatin landscape induced by HFD-feeding are maintained as open chromatin positions for a long time, suggesting that HFD-feeding leads to long-term reprograming of ATMs and renders them prone to pro-angiogenic and pro-inflammatory responses.

ORGANISM(S): Mus musculus

PROVIDER: GSE175614 | GEO | 2024/01/25

REPOSITORIES: GEO

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Adipose tissue stromal cells from lean, obese, and formerly obese mice

Project description:Adipose tissue stromal cells contribute to the regulation of adipose tissue in lean and obese states. Myeloid cells such as adipose tissue macrophages (ATMs) and dendritic cells (ATDCs) undergo both quantitative and qualitative changes with obesity. Due to similarity in markers the identify of adipose tissue dendritic cells and macrophages has been elusive. We have refined prior protocols to unambiguously discern ATM and ATDC in mice. We used microarrays to compare the profiles of ATMs and ATDC from gonadal adipose tissue from lean, obese, and formerly obese mice. We also isolated preadipocytes (PA) from lean and obese mice for comparison. Male C57Bl/6 mice were fed normal diet (ND) or high fat diet (HFD) for 16 weeks. Weight loss (WL) mice were switched from the HFD to ND for 8 weeks. RNA was purified from FACS sorted cell populations (live cells only) obtained from gonadal/epididymal adipose tissue depots. ATMs were defined as CD11c+ (CD45+CD64+ CD11c+) or CD11c- (CD45+CD64+ CD11c-) ATMs. ATDC were defined as CD64- CD11c+. PA were defined as CD31- CD45- Sca1+ PDGFRA+.

2016-09-01 | GSE85846 | GEO

Weight loss resulted in increased expression of the anti-inflammatory protein, CRISPLD2, in mouse adipose tissue

Project description:Purpose: NGS was used to determine if a distinct transcriptomic profile is observed between lean, obese and weight loss fat Methods: We carried out RNA-Seq analysis of epididymal adipose mice ad libitum fed for 10 weeks either a high fat diet (HFD) or a regular chow diet (RD), versus a cohort of mice fed HFD for the first 5 weeks before swapping to RD for the remainder (SWAP). Results: SWAP feeding resulted in weight loss with a parallel improvement in insulin sensitivity. RNA-Seq revealed several transcriptomic signatures distinct to SWAP adipose, distinguished from both RD and HFD adipose. We found a unique up-regulated mRNA encoding a secreted, LPS-binding glycoprotein, CRISPLD2, in SWAP adipose tissue. While cellular CRISPLD2 protein levels were unchanged, plasma CRIPSLD2 levels increased in SWAP mice following weight loss, and can correlate with insulin sensitivity. Conclusions: Taken together, our data demonstrate that CRISPLD2 is a circulating adipokine that may regulate adipocyte remodeling during weight loss.

2019-08-02 | GSE135239 | GEO

MicroRNA-223 ameliorates nonalcoholic steatohepatitis and cancer by targeting multiple inflammatory and oncogenic genes in hepatocytes

Project description:Here, we found that microRNA-223 (miR-223) was highly elevated in hepatocytes after high fat diet (HFD) feeding in mice and in human nonalcoholic steatohepatitis (NASH) samples. Genetic deletion of the miR-223 induced a full spectrum of nonalcoholic fatty liver disease (NAFLD) in mice after long-term (up to one year) HFD feeding including NASH-related steatosis, inflammation, fibrosis and HCC. To better explore the mechanisms underlying the abnormalities observed in HFD-fed miR-223KO mice, we examined hepatic gene expression in 3-month-HFD-fed WT and miR-223KO mice by microarray analysis. Finally, we revealed that miR-223 plays a key role in controlling steatosis-to-NASH progression by inhibiting hepatic Cxcl10 and Taz expression.

2019-03-30 | GSE129080 | GEO

Lactational exposure to high fat diet

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2023-12-08 | GSE227337 | GEO

Genome-wide analysis of gene expression in adipose tissue of female mice after continuous high fat diet feeding

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2013-05-10 | E-GEOD-37238 | biostudies-arrayexpress

Hepatic tissue expression profiles of insulin-sensitive obese mice, insulin-resistant mice and control mice

Project description:Male C57BL/6J mice were fed a high-fat diet (HFD, 60 kcal% fat, D12492, Research Diets, Inc) or normal standard chow diet with 10 kal% fat (ND, D09100304, Research Diets, Inc). Specifically, 6-week-old mice were fed a HFD for 12 weeks to induce insulin resistance (HFD-12w group); 14-week-old mice were fed a HFD for 4 weeks to induce obesity (HFD-4w group). Control mice were fed a ND continuously for 12 weeks starting at 6 weeks of age (ND group). All mice reached the experimental endpoint at 18 weeks of age. Insulin sensitivity was measured by glucose tolerance test and insulin tolerance test. Mice that developed insulin resistance in HFD-12w group and obese mice with normal insulin sensitivity in HFD-4w group were used for further experiments. Mice in ND group were used as controls. Upon reaching the experimental endpoint, livers from three insulin-resistant mice, three insulin-sensitive obese mice, and three control mice were removed for RNA sequencing.

2023-10-14 | GSE245301 | GEO

Transcriptomic profiling of regulatory effects of quercetin and resveratrol supplementation in high fat diet fed mice

Project description:To systemically evaluate the comprehensive alterations under the supplements of quercetin and/or resveratrol in high fat diet (HFD) fed mice, we have employed whole genome microarray expression profiling as a discovery platform to identify genes that differentially altered by different treatments. Gene expression profiles were significantly altered by long term HFD feeding. However, quercetin, resveratrol and their combination could effectively attenuate this alteration. Especially, combination use of quercetin and resveratrol showed more signifcant benefits on the changes of genes, involved in metabolic disorders, induced by HFD, which revealed a synergistic effect of quercetin and resveratrol supplementation in high fat diet fed mice.

2015-05-30 | GSE38325 | GEO

Gene expression profiling from high-fat diet (HFD)-treated and regular diet (RD)-treated lung cancer

Project description:We utilized inducible transgenic mouse with spontaneous lung cancer formation driven by mutant EGFR (by Doxycycline induction) for experiments. Mice fed with regular diet (RD) or high-fat diet (HFD) were induced lung cancer followed by tumor burden evaluation. Lung tissues were harvested for whole-genome transcriptomic, gene enrichment analysis, and cytokine array for potential signatures identification.Gene set enrichment analysis showed the whole-genome transcriptome in HFD vs. RD treated lung cancer was enriched in immune responses and cytokine stimulus.

2018-09-08 | GSE119649 | GEO

Deletion of adipocyte prohibitin 1 exacerbates high-fat diet-induced steatosis but not liver inflammation and fibrosis

Project description:Adipose tissue dysfunction is closely associated with the development and progression of nonalcoholic fatty liver disease (NAFLD). Recent studies have implied an important role of prohibitin-1 (PHB1) in adipose tissue function. In the current study, we aimed to explore the function of adipocyte PHB1 in the development and progression of NAFLD. The PHB1 protein levels in adipose tissues were markedly decreased in mice fed a high-fat diet (HFD) compared to those fed a chow diet. To explore the function of adipocyte PHB1 in the progression of NAFLD, mice with adipocyte-specific (adipo) deletion of Phb1 (Phb1adipo-/- mice) were generated. Notably, Phb1adipo-/- mice did not develop obesity but displayed severe liver steatosis under HFD feeding. Compared to HFD-fed wild-type (WT) mice, HFD-fed Phb1adipo-/- mice displayed dramatically lower fat mass with significantly decreased levels of total adipose tissue inflammation, including macrophage and neutrophil number as well as the expression of inflammatory mediators. To our surprise, although liver steatosis in Phb1adipo-/- mice was much more severe, liver inflammation and fibrosis were similar to WT mice after HFD feeding. RNA sequencing analyses revealed that the interferon pathway was markedly suppressed while the bone morphogenetic protein 2 pathway was significantly up-regulated in the liver of HFD-fed Phb1adipo-/- mice compared with HFD-fed WT mice. Conclusion: HFD-fed Phb1adipo-/- mice display a subtype of the lean NAFLD phenotype with severe hepatic steatosis despite low adipose mass. This subtype of the lean NAFLD phenotype has similar inflammation and fibrosis as obese NAFLD in HFD-fed WT mice; this is partially due to reduced total adipose tissue inflammation and the hepatic interferon pathway.

2022-09-17 | GSE213355 | GEO

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Project description:Gaining understanding of common complex diseases and their treatments are the main drivers for life sciences. As we show here, comprehensive protein set analyses offer new opportunities to decipher functional molecular networks of diseases and assess the efficacy and side-effects of treatments in vivo. Using mass spectrometry, we quantitatively detected several thousands of proteins and observed significant changes in protein pathways that were (dys-) regulated in diet-induced obesity mice. Analysis of the expression and post-translational modifications of proteins in various peripheral metabolic target tissues including adipose, heart, and liver tissue generated functional insights in the regulation of cell and tissue homeostasis during high-fat diet feeding and medication with two antidiabetic compounds. Protein set analyses singled out pathways for functional characterization, and indicated, for example, early-on potential cardiovascular complication of the diabetes drug rosiglitazone. In vivo protein set detection can provide new avenues for monitoring complex disease processes, and for evaluating preclinical drug candidates. Male C57BL/6 mice (age 6 wks) were fed for 12 weeks with high-fat diet (HFD) and than distributed into 3 groups. Mice were than fed over 3 weeks with HFD without compound ('HFD'), HFD with 4 mg/kg/d rosiglitazone ('HFD_RSG') or with 100 mg/kg/d amorfrutin 1 ('HFD_A1'). In parallel, mice were fed for 15 weeks with low-fat diet (LFD) as healthy control subjects. In addition, a group of mice was treated with 37 mg/kg/d amorfrutin 1 during the whole 15 weeks of HFD feeding ('HFD+A1prev'). Finally, visceral white adipose tissue (WAT) was harvested and RNA extracted. --> 2-4 biological replicates (2 mice per each replicate, RNA of 2 mice always pooled).

2013-09-05 | E-GEOD-38855 | biostudies-arrayexpress

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