Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gut microbiota ameliorates hepatic fibrosis through modulating intestinal bile acid metabolism and hepatocyte pyroptosis (Hepatic fibrosis feces)

ABSTRACT:

Hepatic fibrosis decreased feces bile acid level. Hepatic fibrosis increased serum bile acid. This result showed that hepatic fibrosis inhibited the excretion of bile acid in clinical patients. This result provided phenotype for hepatic fibrosis patients. Bile acid was important indexes for liver injury. TCDCA was important, and it play toxicity effect through ferroptosis and apoptosis. The research for other bile acid such CA, UDCA, TUDCA, TDCA, LCA, TLCA would be important.

Hepatic fibrosis feces (sample 2) analysis is reported in the current study MTBLS6742.

Hepatic fibrosis serum (sample 1) analysis is reported in MTBLS6732.

Hepatic fibrosis serum+feces (sample 3) analysis is reported in MTBLS6728.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse phase, Liquid Chromatography MS - positive - reverse phase

SUBMITTER: Qi Zhao

PROVIDER: MTBLS6742 | MetaboLights | 2023-03-17

REPOSITORIES: MetaboLights

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	MTBLS6742	Other
	FILES	Other
	a_MTBLS6742_LC-MS_negative_reverse-phase_metabolite_profiling.txt	Txt
	a_MTBLS6742_LC-MS_positive_reverse-phase_metabolite_profiling.txt	Txt
	files-all.json	Other

Items per page:

1 - 5 of 8

Similar Datasets

Gut microbiota ameliorates hepatic fibrosis through modulating intestinal bile acid metabolism and hepatocyte pyroptosis (Hepatic fibrosis serum)

Project description:Hepatic fibrosis decreased feces bile acid level. Hepatic fibrosis increased serum bile acid. This result showed that hepatic fibrosis inhibited the excretion of bile acid in clinical patients. This result provided phenotype for hepatic fibrosis patients. Bile acid was important indexes for liver injury. TCDCA was important, and it play toxicity effect through ferroptosis and apoptosis. The research for other bile acid such CA, UDCA, TUDCA, TDCA, LCA, TLCA would be important. Hepatic fibrosis serum (sample 1) analysis is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS6732' rel='noopener noreferrer' target='_blank'>MTBLS6732</a>.Hepatic fibrosis feces (sample 2) analysis is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6742' rel='noopener noreferrer' target='_blank'>MTBLS6742</a>.Hepatic fibrosis serum+feces (sample 3) analysis is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6728' rel='noopener noreferrer' target='_blank'>MTBLS6728</a>.

2023-03-17 | MTBLS6732 | MetaboLights

Gut microbiota ameliorates hepatic fibrosis through modulating intestinal bile acid metabolism and hepatocyte pyroptosis (Hepatic fibrosis serum+feces)

Project description:Parabacteroides distasonis (P. distasonis) plays an important role in human health, including diabetes, colorectal cancer and inflammatory bowel disease. Here, we show that P. distasonis is decreased in patients with hepatic fibrosis, and that administration of P. distasonis to mice improves thioacetamide (TAA)- and methionine and choline deficient (MCD) diet-induced hepatic fibrosis. P. distasonis was associated with increased bile salt hydrolase (BSH) activity and inhibition of intestinal farnesoid X receptor (FXR) signaling leading to decreased taurochenodeoxycholic acid (TCDCA) levels in liver. The decrease of TCDCA improved activation of hepatic stellate cells (HSCs) through decreasing the mitochondrial permeability transition (MPT)-Caspase-11 pyroptosis pathway. Celastrol was demonstrated as a promoter of P. distasonis, which could inhibit intestinal FXR and increase the excretion of bile acids, leading to decreased hepatic TCDCA and prevention against TAA- and MCD diet-induced hepatic fibrosis. These data suggest that supplementation of P. distasonis may be a promising means to ameliorate hepatic fibrosis. Hepatic fibrosis serum+feces (sample 3) analysis is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS6728' rel='noopener noreferrer' target='_blank'>MTBLS6728</a>.Hepatic fibrosis serum (sample 1) analysis is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6732' rel='noopener noreferrer' target='_blank'>MTBLS6732</a>.Hepatic fibrosis feces (sample 2) analysis is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6742' rel='noopener noreferrer' target='_blank'>MTBLS6742</a>.

2023-03-17 | MTBLS6728 | MetaboLights

Fibrosis-activated transcriptional networks govern hepatocyte reprogramming and intra-hepatic communication in metabolic associated liver fibrosis

Project description:Liver fibrosis is a strong predictor of long-term mortality in patients with non-alcoholic fatty liver disease; yet the mechanisms underlying the progression from the comparatively benign fatty liver state to advanced non-alcoholic steatohepatitis (NASH) and liver fibrosis are incompletely under-stood. Using a cell type-resolved genomics approach, we show that comprehensive alterations in hepatocyte genomic and transcriptional settings during NASH progression, led to a partial loss of hepatocyte identity. The hepatocyte reprogramming was under tight cooperative control of a net-work of NASH-activated transcription factors (TFs), as exemplified by Elf3 and Glis2. Indeed, Elf3 and Glis2 controlled hepatocyte identity and fibrosis-dependent hepatokine genes targeting disease-associated hepatic stellate cell (HSC) gene programs. Thus, interconnected TF networks not only promoted hepatocyte dysfunction, but also directed the intra-hepatic crosstalk with HSCs necessary for NASH and fibrosis progression implying molecular “hub-centered” targeting strategies to be superior to existing mono-target approaches as currently used in NASH therapy.

2021-07-13 | PXD025691 | Pride

Next Generation Sequencing Facilitates Quantitative Analysis of miRNAs in hepatic fibrosis and normal tissues.

Project description:Aim: Hepatic fibrosis is a major worldwide medical problem and can develop into liver cirrhosis and hepatocellular carcinoma(HCC). Until now, there are no effective drugs for liver ?brosis because the molecular mechanism of progression of liver fibrosis is not fully understood. MicroRNAs (miRNAs) are an important class of small non-coding functional RNAs that play a key role in many biological processes. The purpose of this study was to clarify how the aberrant expression of miRNAs participates in development of the liver fibrosis in rat liver fibrosis model. Methods: Fibrotic and paired normal liver tissues were collected and assesssed by deep sequencing technology. MiRNA pro?ling results were validated by quantitative real-time polymerase chain reaction (qRT-PCR) and bioinformatics was used to predict miRNA targets. Results: Nine deregulated miRNAs were induced in porcine serum (PS)-induced hepatic fibrosis versus normal liver. Further analysis revealed several signaling pathways (e.g., gap junction and neuroactive ligand-receptor interaction) may be associated with hepatic fibrogenesis. Conclusion: Several miRNAs are dysregulated in PS-induced hepatic fibrosis and seem to be closely associated with hepatic fibrogenesis. These results provide an experimental basis for understanding the mechanism of hepatic fibrosis. We sequenced two samples, including case and control. Each sample has two replicates.

2015-06-04 | E-GEOD-54028 | biostudies-arrayexpress

A time-course study of bile duct ligation (BDL)-induced liver fibrosis in rats

Project description:The aim is to characterize rat liver fibrosis induced by bile duct ligation (BDL). To induce hepatic fibrosis, Male Sprague Dawley rats (9-12 weeks of age and 380-420 g of weight upon arrival, supplied by Beijing Vital River laboratory animal Co., Ltd.) underwent surgery of bile duct ligation (BDL). The bile ducts of Sprague-Dawley rats were ligated after 12 hours of fasting and water deprivation. Rat liver samples were collected from three groups of rats at week 1, 2 and 5 after BDL surgery. Three control groups of rats underwent sham operation, including bile duct mobilization, but without BDL. Three biological replicates were used for each group.

2021-09-29 | E-MTAB-10546 | biostudies-arrayexpress

Whole hepatic transcriptomic analysis of C26 cachectic mice treated or not with cholestyramine

Project description:We found out that bile acid pathways were deeply altered in cachectic mice bearing ectopic tumor, leading to an increase in portal and liver conjugated bile acid levels. Counteracting this increased level in conjugated bile acids using cholestyramine, a bile acid sequestrant, reduced hepatic inflammation in cachectic mice with no impact on steatosis and minor effects on thermogenesis. Hepatic whole transcriptome analysis identified 16 pathways altered in cachectic mice which were counteracted by cholestyramine, pointing out the large contribution of bile acids to hepatic disturbances occurring in cancer cachexia.

2021-02-24 | GSE154219 | GEO

Label-free analysis of HCV-associated hepatic fibrosis

Project description:A differential label-fee proteomics approach was performed using 27 biopsies from patients with HCV-associated hepatic fibrosis. For statistical analysis the patients were grouped into a low and a high fibrosis group. The low fibrosis group contained 13 patients of fibrosis stages 0, 1 and 2, whereas the high fibrosis group contained 14 patients of fibrosis stages 3 and 4 (fibrosis stages according to Batts-Ludwig classification).

2015-03-30 | PXD001474 | Pride

Hepatic Sel1L-Hrd1 ER-associated degradation deficiency leads to intrahepatic cholestasis in mice

Project description:The liver is the central organ critically regulating the balance of the metabolically potent yet toxic bile acids in the body. While genomic association studies have pointed to hepatic Sel1L – a critical component of mammalian Hrd1 ER-associated degradation (ERAD) machinery – as an influencer of serum bile acid levels, physiological relevance and mechanistic insights of ERAD in bile homeostasis remain unexplored. Using hepatocyte-specific Sel1L-deficient mouse models, we report that hepatic Sel1L-Hrd1 ERAD critically manages bile homeostasis in the body. Mice with hepatocyte-specific Sel1L developed intrahepatic cholestasis, with significant overload of bile acids in the liver and circulation under basal condition, and were hypersensitive to dietary bile acid challenge. By contrast, biliary bile acid and phosphatidylcholine levels were reduced, pointing to an export defect from hepatocytes. Unbiased proteomics analysis followed by biochemical assays revealed significant accumulation of the bile-stabilizing phosphatidylcholine exporter ATP-binding cassette 4 (Abcb4) in the ER of Sel1L-deficient livers, a gene associated with Progressive Familial Intrahepatic Cholestasis type III. Indeed, Abcb4 was a substrate of Sel1L-Hrd1 ERAD. Hence, hepatic Sel1L-Hrd1 ERAD maintains bile equilibrium via quality control of Abcb4 maturation in the ER.

2023-03-11 | PXD035243 | Pride

Modulating the gut microbiota by dietary guar gum protects against diet-induced obesity but promotes non-alcoholic steatohepatitis in mice

Project description:Non-alcoholic fatty liver disease (NAFLD) is rapidly becoming the most common liver disease worldwide, yet the pathogenesis of NAFLD is only partially understood. Here, we investigated the role of the gut bacteria in NAFLD by stimulating the gut bacteria via feeding mice the fermentable dietary fiber guar gum and suppressing the gut bacteria via chronic oral administration of antibiotics. Guar gum feeding profoundly altered the gut microbiota composition, in parallel with reduced diet-induced obesity and improved glucose tolerance. Strikingly, despite reducing adipose tissue mass and inflammation, guar gum enhanced hepatic inflammation and fibrosis, concurrent with markedly elevated plasma and hepatic bile acid levels. Consistent with a role of elevated bile acids in the liver phenotype, treatment of mice with taurocholic acid stimulated hepatic inflammation and fibrosis. In contrast to guar gum, chronic oral administration of antibiotics effectively suppressed the gut bacteria, decreased portal secondary bile acid levels, and attenuated hepatic inflammation and fibrosis. Neither guar gum or antibiotics influenced plasma lipopolysaccharide levels. In conclusion, our data indicate a causal link between changes in gut microbiota and hepatic inflammation and fibrosis in a mouse model of NAFLD, possibly via alterations in bile acids.

2017-06-06 | GSE76087 | GEO

Dose-dependent metabolic reprogramming and differential gene expression in TCDD-elicited hepatic fibrosis

Project description:We have previously shown that in response to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-elicited NAFLD progression, central carbon, glutaminolysis and serine/folate metabolism are reprogrammed to support NADPH production and ROS defenses. To further investigate underlying dose-dependent responses associated with TCDD-induced fibrosis, female C57BL/6 mice were gavaged with TCDD every 4 days (d) for 28d or 92d. RNA-Seq, ChIP-Seq (2hr), and 28d metabolomic (urine, serum, and hepatic extract) analyses were conducted with complementary serum marker assessments at 92d. Additional vehicle and 30 µg/kg treatment groups were allowed to recover for 36d following the 92d treatment regimen to examine recovery from TCDD-elicited fibrosis. Histopathology revealed dose-dependent increases in hepatic fat accumulation, inflammation, and periportal collagen deposition at 92d, with increased fibrotic severity in the recovery group. Serum proinflammatory and profibrotic interleukins-1β, -2, -4, -6, and -10, as well as TNFα and IFNγ, exhibited dose-dependent induction. An increase in glucose tolerance was observed with a concomitant 3.0-fold decrease in hepatic glycogen linked to increased ascorbic acid biosynthesis and proline metabolism, consistent with increased fibrosis. RNA-Seq identified differential expression of numerous matrisome genes including an 8.8-fold increase in Tgfb2 indicating myofibroblast activation. Further analysis suggests reprogramming of glycogen, ascorbic acid, and amino acid metabolism in support of collagen deposition and the use of proline as a substrate for ATP production via the proline cycle. Conclusion: In addition to metabolic reprogramming in support of NADPH production for ROS defense, we demonstrate that glycogen, ascorbic acid, and amino acid metabolism are also reorganized to support remodeling of the extracellular matrix, progressing to hepatic fibrosis in response to chronic injury from TCDD.

2016-09-01 | GSE81990 | 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