Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mouse gut metagenome

ABSTRACT: FK506 binding protein 5 deficiency regulates gut microbiome against diet-induced obesity in mice

PROVIDER: PRJNA610239 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11308300_1.fastq.gz	Fastqsanger.gz
	SRR11308300_2.fastq.gz	Fastqsanger.gz
	SRR11308301_1.fastq.gz	Fastqsanger.gz
	SRR11308301_2.fastq.gz	Fastqsanger.gz
	SRR11308302_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 40

Similar Datasets

gut metagenome

Project description:QQ Diet-Induced Obesity

| PRJNA918340 | ENA

Gut Microbe-Targeted Choline Trimethylamine Lyase Inhibitors Improves Obesity Via Rewiring of Host Circadian Rhythms.

Project description:The increasing prevalence of obesity and related metabolic disorders represents a growing public health concern. Despite advances in other areas of medicine, a safe and effective drug treatment for obesity has been elusive. Obesity has repeatedly been linked to reorganization of the gut microbiome 1-4 , yet to this point obesity therapeutics have been targeted exclusively toward the human host. Here we show that gut microbe-targeted inhibition of the metaorganismal trimethylamine N-oxide (TMAO) pathway protects mice against the metabolic disturbances associated with diet-induced obesity (DIO) or leptin deficiency (ob/ob). Selective small molecule inhibition of the gut microbial enzyme choline TMA-lyase (CutC) does not significantly reduce food intake, but instead is associated with beneficial remodeling of the gut microbiome, improvement in glucose tolerance, and enhanced energy expenditure. Leveraging untargeted metabolomics we discovered that CutC inhibition is associated with reorganization of host circadian control of both phosphatidylcholine and energy metabolism. Collectively, this study underscores the close relationship between microbe and host metabolism, and provides evidence that gut microbe-derived trimethylamine (TMA) is a key regulator of the host circadian clock. This work also demonstrates that gut microbe-targeted enzyme inhibitors can have profound effects on host energy metabolism, and have untapped potential as anti-obesity therapeutics.

2021-03-31 | GSE157925 | GEO

Time-dependent network analysis reveals molecular targets underying the development of diet-induced obesity and non-alcoholic steatohepatitis.

Project description:Core diet-induced obesity networks were constructed using Ingenuity pathway analysis (IPA) based on 332 high-fat diet responsive genes identified in liver by time-course microarray analysis (8 time-points over 24 weeks) of high-fat diet fed mice compared to normal diet fed mice. IPA identified five core diet-induced obesity networks with time-dependent gene expression changes in liver. When we merged core diet-induced obesity networks, Tlr2, Cd14 and Ccnd1 emerged as hub genes associated with both liver steatosis and inflammation and were altered in a time-dependent manner. Further protein-protein interaction network analysis revealed Tlr2, Cd14 and Ccnd1 were inter-related through the ErbB/insulin signaling pathway. Dynamic changes occur in molecular networks underlying diet-induced obesity. Tlr2, Cd14 and Ccnd1 appear to be hub genes integrating molecular interactions associated with the development of NASH. Therapeutics targeting hub genes and core diet-induced obesity networks may help ameliorate diet-induced obesity and NASH. Total RNA obtained from isolated liver of C57BL/6J mice fed normal diet or high fat diet for 0, 2, 4, 6, 8, 12, 16, 20 and 24 weeks.

2014-03-01 | E-GEOD-40481 | biostudies-arrayexpress

Time-dependent network analysis reveals molecular targets underying the development of diet-induced obesity and non-alcoholic steatohepatitis.

2014-03-01 | GSE40481 | GEO

Expression data from liver of the KRAP deficient mice

Project description:KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule. KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia.

2009-01-22 | GSE13583 | GEO

Expression data from BAT of the KRAP deficient mice

2009-01-22 | GSE13582 | GEO

mouse gut metagenome

Project description:Interaction of gut microbiota and anti-obesity drugs in diet induced obesity model

| PRJDB12833 | ENA

EBF2 promotes the recruitment of beige adipocytes in white adipose tissue

Project description:The induction of beige/brite adipose cells in white adipose tissue (WAT) is associated with protection against high fat diet-induced obesity and insulin resistance in animals. The helix-loop-helix transcription factor Early B-Cell Factor-2 (EBF2) regulates brown adipose tissue development. We examined the role of EBF2 in beige fat cell biogenesis by comparing transcriptome in wildtype and EBF2-overexpressing mice in the adipose tissue. Four control replicates (wildtype) and four experimental replicates (Fabp4-Ebf2) mice were analyzed

2015-12-31 | E-GEOD-74366 | biostudies-arrayexpress

Project description:Lymphotoxin regulates commensal responses to enable diet-induced obesity

| PRJNA599407 | ENA

Adipocyte YTH N(6)-methyladenosine RNA-binding protein 1 protects against obesity by promoting white adipose tissue beiging in male mice

Project description:Obesity, one of the most serious public health issues, is caused by energy imbalance of energy intake and expenditure. N(6)-methyladenosine (m6A) RNA modification has been recently identified as a key regulator of obesity, while the detailed mechanism is elusive. Here, we found that YTH RNA binding protein 1 (YTHDF1), an m6A reader, acts as an essential regulator of white adipose tissue metabolism. The expression of YTHDF1 decreased in adipose tissue of mice fed a high-fat diet. Adipocyte-specific Ythdf1 deficiency exacerbated obesity-induced metabolic defects and inhibited beiging of inguinal white adipose tissue (iWAT) in mice. By contrast, mice with WAT-specific Ythdf1 overexpression were resistant to obesity and showed promotion of beiging. Mechanistically, YTHDF1 regulated the translation of diverse m6A-modified mRNAs. In particular, YTHDF1 facilitated the translation of bone morphogenetic protein 8b (Bmp8b) in an m6A-dependent manner to induce the beiging process. Together, these findings suggested that YTHDF1 may be an attractive therapeutic target for the management of obesity-associated diseases.

2023-02-02 | GSE197173 | 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