Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bile acid standards for Mouse diet study

ABSTRACT: Bile acid standards were run alongside mouse diet samples to annotate bile acids as Level 1 annotations.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Standards

SUBMITTER: Allegra Aron

PROVIDER: MSV000091347 | MassIVE | Wed Feb 22 12:52:00 GMT 2023

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Bile Acid Standards for MSV000093200

Project description:Bile acid standards run alongside MSV000093200 (Gates Foundation SEPSIS project).

2023-11-02 | MSV000093262 | MassIVE

GNPS - Bile Acid Standards for MSV000093200

Project description:Bile acid standards run alongside MSV000093200 (Gates Foundation SEPSIS project).

2023-11-02 | MSV000093262 | GNPS

A diet-sensitive epigenetic pathway links hepatic bile acid metabolism to cholesterol absorption and atherosclerosis

Project description:Dietary nutrients interact with the gene networks to orchestrate adaptive responses during metabolic stress. Tissue metabolic reprogramming is frequently linked to induction of pathways with pathophysiological consequences. Here we identified Baf60a as a diet-sensitive subunit of the SWI/SNF chromatin-remodeling complexes in the liver that links the consumption of fat- and cholesterol-rich diet to elevated plasma cholesterol levels. The expression of Baf60a in the liver was elevated following western diet feeding. Hepatocyte-specific inactivation of Baf60a reduced bile acid production and intestinal cholesterol absorption, and attenuated diet-induced hypercholesterolemia and atherosclerosis in mice. At the mechanistic level, Baf60a stimulates the expression of hepatic genes involved in bile acid synthesis, modification, and transport through a CAR/Baf60a feedforward regulatory loop. Baf60a is required for the recruitment of the SWI/SNF chromatin-remodeling complexes to facilitate an activating epigenetic switch on the CAR target genes. These studies elucidate an unexpected regulatory pathway that mediates the hyperlipidemic and atherogenic effects of western diet consumption. We used microarrays to elucidate the role of hepatic Baf60a in the regulation of lipid metabolism.

2015-10-03 | GSE73709 | GEO

Diet Modulation of Bacterial Sulfur and Bile Acid Metabolism and Colon Cancer Risk

Project description:Determine in the context of a controlled crossover diet-intervention trial the role of taurocholic acid metabolism by gut bacteria in African American subjects at elevated risk for colorectal cancer (CRC). Two isocaloric diets, an animal-based diet high in taurine and saturated fat (HT-HSAT) and a plant-based, low in taurine and low saturated fat (LT-LSAT) will be used to determine the extent to which the relationship between diet (independent variable) and mucosal markers of CRC risk including epithelial proliferation, oxidative stress, DNA damage, and primary and secondary bile acid pools and biomarkers of inflammation (dependent variables) is explained by the abundance of sulfidogenic bacteria and hydrogen sulfide (H2S) concentrations &/or deoxycholic acid (DCA) and DCA-producing bacteria clostridium scindens (mediator variables).

| 2274903 | ecrin-mdr-crc

Standards of bile acids on Q Exactive

Project description:MS/MS fragmentation data on bile acid standards were acquired on the QE - with a gradient developed to separate between isomeric pairs on a Polar C18 column and a fragmentation energy of NCE 45.

2023-05-22 | MSV000092003 | MassIVE

NUDT7 Regulates Total Hepatic CoA Levels and the Composition of the Intestinal Bile Acid Pool in Male Mice Fed a Western Diet

Project description:Nudix hydrolase 7 (NUDT7) is a peroxisomal (acyl-)CoA-degrading enzyme that is highly expressed in the liver. We previously showed that liver-specific NUDT7 overexpression affects peroxisomal lipid metabolism, but does not prevent the increase in total liver CoA levels that occurs with fasting. Herein, we show that deletion of Nudt7 alters the composition of the hepatic acyl-CoA pool in mice fed a low fat diet, but only in males fed a western diet does the lack of NUDT7 increase total liver CoA levels. This effect is driven by the accumulation of medium-chain dicarboxylic acyl-CoAs, which are products of the oxidation of dicarboxylic fatty acids in the peroxisomes. We also show that, under conditions of increased cholesterol intake and elevated bile acid synthesis, Nudt7 deletion increases the production of tauro-muricholic acids, decreasing the hydrophobicity index of the intestinal bile acid pool and increasing fecal cholesterol excretion. Collectively, our findings reveal a key role for NUDT7 in the regulation of the final products of bile acid synthesis and dicarboxylic fatty acid oxidation

2022-11-25 | GSE207914 | GEO

RNA-seq analysis of livers of mice fed a high fat diet with and without administration of an inhibitor of the ileal bile acid uptake transporter ASBT

Project description:The study was designed to determine the effect of inhibition of ileal bile acid uptake on hepatic gene expression in high fat diet induced hepatic steatosis in mice

2016-09-22 | GSE84994 | GEO

Secondary bile acid production by gut bacteria promotes Western diet-associated colorectal cancer

Project description:Secondary bile acid production by gut bacteria promotes Western diet-associated colorectal cancer

| PRJEB60380 | ENA

Bile acid therapeutics for NASH

Project description:Bile acid therapeutics for NASH

| PRJNA705980 | ENA

Maternal bile acid transporter deficiency promotes neonatal demise

Project description:Intrahepatic cholestasis of pregnancy (ICP) is estimated to impact between 0.4% and 5% of pregnancies worldwide. This disease is associated with elevated maternal bile acids and frequently untoward neonatal outcomes such as respiratory distress and asphyxia. Multiple candidate genes have been implicated, but none have provided insight into the mechanisms of neonatal respiratory distress and death. Herein our studies demonstrate that maternal cholestasis (due to Abcb11 deficiency) produces 100% neonatal death within 24h due to atelectasis producing pulmonary hypoxia, which recapitulates the respiratory distress and asphyxia of human ICP. We show that these neonates have elevated pulmonary bile acids that are associated with disrupted structure of pulmonary surfactant. Maternal absence of Nr1i2 superimposed upon Abcb11 deficiency strongly increased neonatal survival and is directly related to reduced maternal bile acid concentrations. The mechanism accounting for reduced serum bile acids in the mothers deficient in both Nr1i2 and Abcb11 appears related to disrupted reabsorption of intestinal bile acids due to changes in transporter expression. These findings provide novel insights into pulmonary failure by revealing bile acids capability to disrupt the structure of surfactant producing collapsed alveoli, pulmonary failure and ultimately death. These findings have important implications for neonatal health especially when maternal bile acids are elevated during pregnancy and highlight a potential pathway and targets amenable to therapeutic intervention to ameliorate this condition.

2015-09-23 | GSE70179 | 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