Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Magnesum Isoglycyrrhizinate augments lipid catabolism via immune-neuro modulation of catecholamine pathways

ABSTRACT: Magnesum Isoglycyrrhizinate augments lipid catabolism via immune-neuro modulation of catecholamine pathways

PROVIDER: PRJNA1144150 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR30126906_1.fastq.gz	Fastqsanger.gz
	SRR30126906_2.fastq.gz	Fastqsanger.gz
	SRR30126907_1.fastq.gz	Fastqsanger.gz
	SRR30126907_2.fastq.gz	Fastqsanger.gz
	SRR30126908_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Magnesum Isoglycyrrhizinate augments lipid catabolism via immune-neuro modulation of catecholamine pathways

Project description:Glycyrrhetinic acid (GA) and its derivative, magnesium isoglycyrrhizinate, exhibit promising anti-obesity effects through mechanisms that are not fully understood. Here, we showed that GA mitigated white adipose tissue remodeling and diet-induced obesity by enhancing lipid catabolism. GA indirectly promoted adipocyte lipolysis and thermogenesis by modulating catecholamine pathways, facilitated by increased intra-fat sympathetic innervation and reduced protein expression of monoamine oxidase A (MAOA), which degrades norepinephrine. In suit visualization of MAOA identified adipose tissue macrophages (ATMs) as key mediators of intra-fat catecholamine degradation. RNA sequencing of sorted ATMs revealed that GA reduced pro-inflammatory shifts and altered macrophage polarity, preventing activation of the Toll-like receptor 4 (TLR4) signaling pathway, as supported by molecular docking analysis and binding assays. Moreover, the anti-obesity effects of GA were absent in TLR4-deletive mice, which exhibited decreased MAOA protein levels and sensitivity to FUNDC1-mediated mitophagy in ATMs. These findings suggest that GA targets macrophage-sympathetic neuron crosstalk, offering a promising therapeutic approach for obesity by preserving NE availability and promoting lipid catabolism.

2024-10-01 | GSE273958 | GEO

Infiltration of monocyte-derived macrophages perturbs the CNS metabolic landscape, licensing arginine catabolism and augments neuro-inflammation

Project description:Infiltration of monocyte-derived macrophages perturbs the CNS metabolic landscape, licensing arginine catabolism and augments neuro-inflammation

| PRJNA966117 | ENA

Increased Neanderthal ancestry in genomic regions associated with lipid catabolism in contemporary Europeans

Project description:While Neanderthals are extinct, fragments of their genome still persist in the genomes of contemporary humans. Here, we show that such Neanderthal-like sequences are not distributed randomly in contemporary human genomes. Specifically, while genome-wide frequency of Neanderthal-like sites is close to 6% in all out-of-Africa populations, genes involved in lipid catabolism contain large excess Neanderthal-like sequences in Europeans (24.3%), but not in Asians (12.4%). While lipid catabolism cannot be assayed in Neanderthals, we took advantage of genetic divergence between human populations, chimpanzees and Neanderthals to predict metabolic divergence expected from the observed excess of Neanderthal gene flow into Europeans. We confirmed predicted changes in lipid catabolism using hydrophobic metabolome measurements in the brain tissue and further linked these metabolic changes to gene expression divergence. 14 human and 6 chimpanzee samples were sequenced.

2014-03-31 | E-GEOD-45263 | biostudies-arrayexpress

Increased Neanderthal ancestry in genomic regions associated with lipid catabolism in contemporary Europeans

2014-03-31 | GSE45263 | GEO

Light augments antidepressant response via astroglial modulation of lateral habenula

Project description:Light augments antidepressant response via astroglial modulation of lateral habenula

| PRJNA601773 | ENA

The class 3 PI3K coordinates autophagy and mitochondrial lipid catabolism by controlling nuclear receptor PPARα

Project description:The class 3 phosphoinositide 3-kinase (PI3K) is required for the lysosomal degradation by autophagy and vesicular trafficking, assuring adaptation to energy shortages. Mitochondrial lipid catabolism is another important energy source. Autophagy and mitochondrial metabolism are transcriptionally controlled by nutrient sensing nuclear receptors. However, it is not known whether the class 3 PI3K contributes to this regulation. Here we show that hepatocyte-specific inactivation of Vps15, the essential regulatory subunit of the class 3 PI3K, results in mitochondrial depletion and a failure to oxidize fatty acids. Mechanistically, the transcriptional activity of Peroxisome Proliferator Activated Receptor alpha (PPARα), a nuclear receptor that orchestrates fatty acid catabolism, is blunted in Vps15-deficient livers. We find PPARα transcriptional repressors Histone Deacetylase 3 (Hdac3) and Nuclear receptor co-repressor 1 (NCoR1) accumulated in Vps15-deficient livers due to defective autophagic flux. Pharmacologic activation of PPARα with a synthetic ligand, re-expression of its co-activator Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha (PGC-1α) or inhibition of Hdac3 restored mitochondrial biogenesis and lipid oxidation in Vps15-deficient hepatocytes. These findings reveal a role for the class 3 PI3K and autophagy in transcriptional coordination of mitochondrial metabolism.

2020-02-06 | E-MTAB-7685 | biostudies-arrayexpress

Neuro-Glioblastoma Connectivity: Brain-Wide Mapping and Cholinergic Modulation of Tumor Progression

Project description:Neuro-Glioblastoma Connectivity: Brain-Wide Mapping and Cholinergic Modulation of Tumor Progression

| PRJNA1281079 | ENA

Increased Neanderthal ancestry in genomic regions associated with lipid catabolism in contemporary Europeans

Project description:Increased Neanderthal ancestry in genomic regions associated with lipid catabolism in contemporary Europeans

| PRJNA193342 | ENA

Lipid catabolism inhibition sensitizes prostate cancer cells to antiandrogen blockade

Project description:Prostate cancer (PCa) is the most common malignancy among western men and the second leading-cause of cancer related deaths. For men who develop metastatic, castration-resistant PCa (mCRPC), survival is limited, making the identification of novel therapies for mCRPC critical. Deficient lipid oxidation via carnitine palmitoyltransferase (CPT1) results in decreased growth and invasion, underscoring the role of lipid catabolism to fuel PCa growth. In fact, the CPT1A isoform is abundant in PCa, especially in those with high-grade tumors. Since lipid oxidation is stimulated by androgens, we have evaluated the synergistic effects of combining CPT1A inhibition and anti-androgen therapy. Mechanistically, we have found that decreased CPT1A expression is associated with decreased AKT content and activation, likely driven by a breakdown of membrane phospholipids and activation of the INPP5K phosphatase. This results in increased AR content and increased sensitivity to the anti-androgen enzalutamide. To better understand the clinical implications of this findings, we have evaluated fat oxidation inhibitors (etomoxir, ranolazine and perhexiline) in combination with enzalutamide in PCa cell models. We have observed a robust inhibitory effect of the combinations, including in enzalutamide-resistant cells and mouse TRAMPC1 cells, a more neuroendocrine PCa model. Lastly, using a xenograft mouse model, we have observed decreased tumor growth with a systemic combination treatment of enzalutamide and ranolazine. In conclusion, our results show that improved anti-cancer efficacy can be achieved by co-targeting the AR axis and fat oxidation via CPT1A, which may have clinical implications, especially in the mCRPC setting.

2017-06-10 | GSE83547 | GEO

Characterisation of p-hydroxycinnamate catabolism in a soil Actinobacterum

Project description:p-Hydroxycinnamates, such as p-coumarate and ferulate, are components of plant cell walls and have a number of commercial applications. Previously, we had shown that the soil Actinobacterium Rhodococcus jostii RHA1 (RHA1) grows on ferulate, catabolizing it via vanillate and the M-NM-2-ketoadipate pathway. We used transcriptomics to identify genes in RHA1 that were specifically up-regulated during growth on ferulate. These include three operons predicted to encode the uptake and M-NM-2-oxidative deacetylation of ferulate and p-coumarate: couHLT, couMNO and couR. A couL mutant did not grow on p-coumarate, ferulate or their dihydro derivatives, but grew on vanillate. Purified CouL catalyzed the thioesterification of several p-hydroxycinnamates. Among the tested substrates, the best were p-coumarate and caffeate (kcat/KM ~400 mM-1s-1), and sinapate was not transformed. Of these, p-coumarate was also RHA1M-bM-^@M-^Ys preferred growth substrate. Although the data indicate that p-hydroxycinnamates are catabolized via M-NM-2-oxidation, the pathway lacks a typical M-NM-2-ketothiolase. The data further suggest the involvement of two formaldehyde detoxification pathways in vanillate catabolism. This study augments our understanding of the bacterial catabolism of biomass and facilitates the production of aromatics from renewable feedstocks. Transcriptomes of R. jostii RHA1 from ferulate and benzoate cultures were analysed using Ion PGMTM system.

2014-09-28 | E-GEOD-56355 | biostudies-arrayexpress

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