Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

High-Fat Diet-Induced Liver-Gut Crosstalk Suppresses Autophagy and Exacerbates Colitis [liver]

ABSTRACT: The goal of this project is to investigate the mechanisms through which high fat diet (HFD) exacerbates colitis via the liver-gut axis, particularly focusing on liver dysregulated lipid metabolism and intestinal autophagy. We examined liver transcriptomes of C57BL6/J mice fed a control diet (CD) or HFD with or without dextran sulfate sodium (DSS) by RNA seq analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE293183 | GEO | 2025/04/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

High-Fat Diet-Induced Liver-Gut Crosstalk Suppresses Autophagy and Exacerbates Colitis [colon]

Project description:The goal of this project is to investigate the mechanisms through which high fat diet (HFD) exacerbates colitis via the liver-gut axis, particularly focusing on liver dysregulated lipid metabolism and intestinal autophagy. We examined colon transcriptomes of C57BL6/J mice fed a control diet (CD) or HFD with or without dextran sulfate sodium (DSS) by RNA seq analysis.

2025-07-02 | GSE293222 | GEO

High-Fat Diet-Induced Liver-Gut Crosstalk Suppresses Autophagy and Exacerbates Colitis [liver]

Project description:High-Fat Diet-Induced Liver-Gut Crosstalk Suppresses Autophagy and Exacerbates Colitis [liver]

| PRJNA1243316 | ENA

Proteomics reveals PFOS-induced alteration of lipid utilization and xenobiotic metabolism in a model of PFOS-augmented diet-induced fatty liver

Project description:Perfluorooctanesulfonic acid (PFOS) is a persistent, bio-accumulative pollutant that has been used for the last 60+ years in numerous industrial and commercial applications. In mice, PFOS administration is known to induce hepatomegaly and hepatic steatosis. The aim of the present study was to evaluate potential PFOS and diet interactions and explore the mechanism of PFOS induced liver lipid accumulation. Prior to PFOS administration, mice were fed either a standard chow diet (SD) or 60% kCal high fat diet (HFD) for 4 weeks to establish significant body weight increase. After 4 weeks of diet acclimation, the treatment groups received 0.0003% PFOS in diet for an additional 10 weeks. In addition, a subset of the mice fed HFD were switched to a SD (H-SD) to mimic weight-loss induced improvement of hepatic steatosis. A total of six treatment groups: i) SD, ii) HSD, iii) HFD (H), iv) SD +PFOS(SDP), v) H-SD +PFOS (HSDP), and vi) HFD +PFOS (HP) were included. PFOS and lipid concentrations were measured in both serum and liver. Relative liver mRNA expression was determined by targeted bead array and proteins were quantified using untargeted mass spectrometry. PFOS exposure increased liver weight, and in the HFD increased liver triglycerides and liver cholesterol content. Gene and protein expression in the liver demonstrated that PFOS exposure induced lipid utilization and xenobiotic metabolism pathways, and in a HFD, induced lipid synthesis. The data suggests that PFOS exposure acts on lipid utilization genes and exacerbates hepatic steatosis in mice fed a HFD.

2020-09-30 | PXD016161 | Pride

High-Fat Diet-Induced Liver-Gut Crosstalk Suppresses Autophagy and Exacerbates Colitis [colon]

Project description:High-Fat Diet-Induced Liver-Gut Crosstalk Suppresses Autophagy and Exacerbates Colitis [colon]

| PRJNA1243378 | ENA

Expression data for eidididymal fat from high fat diet mice.

Project description:Using a C57BL6/J mouse model of diet-induced obesit,we observed that mannose supplementation of high fat diet (HFD)-fed mice prevents weight gain,lowers adiposity, reduces liver steatosis, and improves glucose tolerance and insulin sensitivity. We used microarrays to determine the gene expression pattern in epididymal fat frommice weaned on Normal diet (ND), HFD and HFD with mannose (HFDM)

2018-11-06 | GSE110333 | 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

Multigenerational paternal high-fat diet gradually exacerbates environmental stress-induced testicular dysregulated expression of mRNAs in offspring

Project description:To investigate the mechanism by which paternal exposure to high-fat diet (HFD) exacerbates environmental stress-impaired testicular germ cell development in offspring, testicular RNA sequencing was performed in H+Cd (the offspring were treated with Cd after paternal exposure to one-generational HFD) and H+H+Cd (the offspring were treated with Cd after paternal exposure to bi-generational HFD) groups. Compared with HFD1D group and HFD2D group, 229 mRNAs were upregulated and 268 mRNAs were downregulated, screened for a 1.2-fold change and adjusted with P < 0.05. GO analysis revealed that downregulated mRNAs were related to multiple biological processes, including the "retinol metabolic process," the "reproductive process," and the "spermatogenesis".

2023-12-22 | GSE241413 | GEO

high fat diet feed mice liver sample proteomics

Project description:determine the effect of the high-fat diet on the proteomics profile of liver tissue.Mice were fed with HFD for 16 weeks to establish a NAFLD mouse model. Mice fed with normal chow diet were taken as controls. Five replicate liver samples were collected from each group for proteomics analysis.

2022-06-09 | PXD030727 | Pride

Cullin-associated and neddylation-dissociated protein 1 (CAND1) alleviates NAFLD by reducing ubiquitinated degradation of ACAA2

Project description:Nonalcoholic fatty liver disease (NAFLD) is the most common liver disorder with high morbidity and mortality. The current study aims to explore the role of Cullin-associated and neddylation-dissociated protein 1 (CAND1) in the development of NAFLD and the underlying mechanisms. CAND1 is reduced in the liver of NAFLD male patients and high fat diet (HFD)-fed male mice. CAND1 alleviates palmitate (PA) induced lipid accumulation in vitro. Hepatocyte-specific knockout of CAND1 exacerbates HFD-induced liver injury in HFD-fed male mice, while hepatocyte-specific knockin of CAND1 ameliorates these pathological changes. Mechanistically, deficiency of CAND1 enhances the assembly of Cullin1, F-box only protein 42 (FBXO42) and acetyl-CoA acyltransferase 2 (ACAA2) complexes, and thus promotes the ubiquitinated degradation of ACAA2. ACAA2 overexpression abolishes the exacerbated effects of CAND1 deficiency on NAFLD. Additionally, androgen receptor binds to the -187 to -2000 promoter region of CAND1. Collectively, CAND1 mitigates NAFLD by inhibiting Cullin1/FBXO42 mediated ACAA2 degradation

2023-10-24 | PXD043719 | Pride

Expression data from epidermal stem cells from young mice fed either with normal diet or high fat diet

Project description:High fat diet (HFD), if prolonged, leads to obesity thereby accelerating the development of many ageing-related pathologies including chronic inflammation, cardiovascular disease, diabetes, and a higher predisposition to develop cancer. We asked whether HFD could reprogram the circadian output of young stem cells in a manner similar to what we observed during physiological ageing. HFD has been recently shown to induce a rewiring of the liver circadian transcriptome and metabolome, although in an obesity-independent manner. We therefore fed young (8 week old) C57Bl6 mice with HFD or its control diet for 7-weeks, a time when mice had not yet become obese, and performed circadian transcriptome analysis.

2017-08-10 | GSE84510 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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