Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Porphyran from discolored nori prevents metabolic syndrome through microbiota-bile acid-ceramide pathway

ABSTRACT: Porphyran from discolored nori prevents metabolic syndrome through microbiota-bile acid-ceramide pathway

PROVIDER: PRJNA700967 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Porphyran from discolored nori prevents metabolic syndrome through microbiota-bile acid-ceramide pathway

Project description:To investigate nori (seaweed) effects on metabolic syndrome, we conducted microarray analysis.

2025-05-19 | GSE166440 | GEO

Porphyran from discolored nori prevents metabolic syndrome through microbiota-bile acid-ceramide pathway.

Project description: Not available

| S-EPMC12148601 | biostudies-literature

Ursodeoxycholic acid alleviates aortic aneurysm and dissection through the intestinal farnesoid X receptor/ceramide synthesis 2 axis

Project description:The farnesoid X receptor (FXR) is a nuclear receptor mainly expressed in the liver and intestine. In the intestine, FXR plays a crucial role in regulating lipid metabolism, bile acid homeostasis, and intestinal barrier function.Activation of FXR can lead to the regulation of a variety of genes involved in these processes. For example, it can affect the absorption and transport of lipids and bile acids through the intestine,in this paper,we Ursodeoxycholic acid alleviates aortic aneurysm and dissection through the intestinal farnesoid X receptor/ceramide synthesis 2 axis.

2025-05-10 | GSE280869 | GEO

Bile acid receptor Tgr5 prevents macrophage hyperinflammation during bacterial sepsis through metabolic and epigenetic silencing

Project description:Bile acid receptor Tgr5 prevents macrophage hyperinflammation during bacterial sepsis through metabolic and epigenetic silencing

| PRJNA1336054 | ENA

Bile acid receptor Tgr5 prevents macrophage hyperinflammation during bacterial sepsis through metabolic and epigenetic silencing

Project description:Tgr5 is a membrane-bound bile acid receptor that negatively regulates immune cells, although the molecular mechanisms behind this observation remain elusive. Here we report that Tgr5 is upregulated in macrophages during stimulation with Listeria monocytogenes and that Tgr5-deficient macrophages are hyperinflammatory and mice with myeloid Tgr5 deficiency are more susceptible to Listeria monocytogenes sepsis. Unexpectedly, Tgr5-deficient macrophages show reduced glycolysis and ATP citrate lyase expression, which cumulates in Acetyl-CoA deficiency and metabolic-epigenetic gene silencing, driving macrophages towards a hyperinflammatory phenotype during bacterial sepsis

2025-10-03 | GSE309415 | GEO

Platycodi Radix Extract Prevents Hepatic Steatosis by Enhancing Bile Acid Synthesis in a High-Fat Diet-Induced Fatty Liver Mouse Model

Project description:This project investigated the molecular mechanism by which *Platycodi Radix* extract (PRE; the ethanol extract of the root of *Platycodon grandiflorum*) prevents non-alcoholic fatty liver disease (NAFLD) in a high-fat diet (HFD)-induced fatty liver mouse model, using a liver-tissue shotgun proteomic and bioinformatic approach. Five-week-old male C57BL/6J mice were acclimatized and then maintained for 12 weeks on one of three diets: a normal chow diet (NCD), a high-fat diet (HFD), or an HFD supplemented with 5% (w/w) PRE. PRE supplementation prevented HFD-induced body-weight gain, fat accumulation, and hepatic steatosis, and improved glucose tolerance and serum lipid profiles. To elucidate the underlying mechanism, liver proteomes of the NCD, HFD, and PRE groups were profiled by LC-MS/MS (n = 3 per group), and proteins differing in relative abundance between NCD vs HFD and HFD vs PRE were interpreted by Ingenuity Pathway Analysis. This LC-MS/MS dataset was designed as a discovery-stage, exploratory screen for hypothesis generation rather than as standalone quantitative proof of differential expression; the resulting candidate proteins and pathways (notably decreased FXR/RXR-activation proteins and increased cholesterol-biosynthesis proteins, predicting enhanced bile-acid synthesis) were subsequently validated by targeted Western blotting and biochemical bile-acid measurement, on which the mechanistic conclusions of the study are based. This dataset comprises the liver-tissue LC-MS/MS data and the protein identification/quantification results supporting the conclusion that PRE prevents hepatic steatosis through modulation of FXR/RXR activation, cholesterol biosynthesis, and bile-acid synthesis pathways.

2026-07-04 | PXD080181 | Pride

Metabolic surgery reduces CRC disease progression mediated by circulating bile acid diversion

Project description:Tumor organoids of a patient with microsatellite stable (MSS) colorectal cancer were co-incubated with primary bile acids (CA, GCA, TCA; 100 µM) to analyze the effect of bile acids on tumorigenesis of colorectal cancer.

2026-06-01 | GSE298489 | GEO

Liver-specific ceramide reduction alleviates steatosis and insulin resistance in alcohol-fed mice

Project description:Alcohol’s impairment of both hepatic lipid metabolism and insulin resistance (IR) are key drivers of alcoholic steatosis, the initial stage of alcoholic liver disease (ALD). Pharmacologic reduction of lipotoxic ceramide prevents alcoholic steatosis and glucose intolerance in mice, but potential off-target effects limit its strategic utility. Here, we employed a hepatic-specific acid-ceramidase (ASAH) overexpression model to reduce hepatic ceramides in a Lieber-DeCarli model of experimental alcoholic steatosis. We examined effects of alcohol on hepatic lipid metabolism, body composition, energy homeostasis and insulin sensitivity as measured by hyperinsulinemic-euglycemic clamp. Our results demonstrate that hepatic ceramide reduction ameliorates the effects of alcohol on hepatic lipid droplet accumulation by promoting VLDL secretion and lipophagy, the latter of which involves ceramide cross-talk between the lysosomal and lipid droplet compartments. We additionally demonstrate that hepatic ceramide reduction prevents alcohol’s inhibition of hepatic insulin signaling. These effects on the liver are associated with a reduction in oxidative stress markers and are relevant to humans, as we observe peri-lipid droplet ASAH expression in human ALD. Together, our results suggest a potential role for hepatic ceramide inhibition in preventing ALD.

2020-07-08 | GSE139015 | GEO

Intestinal Epithelial Tet2 Deficiency Reprograms the Gut Microbiota through Bile Acid Metabolic Alterations

Project description:Epigenetic mechanisms are increasingly recognized as critical regulators of host-microbiota interactions. Here, we report that intestinal epithelial-specific deletion of Tet2, a key DNA demethylase, leads to structural abnormalities, impaired barrier function, and remarkable reprogramming of the gut microbial community. Mechanistically, Tet2 deficiency significantly downregulated the expression of the apical sodium-dependent bile acid transporter (ASBT/Slc10a2), resulting in altered bile acid homeostasis with specific accumulation of hyocholic acid (HCA) in the intestinal lumen. This metabolic shift created a favorable niche for selective expansion of bile salt hydrolase (BSH)-expressing Lactobacillus species. Furthermore, we identified an age-dependent regulatory role of HCA in shaping microbial composition, promoting Lactobacillus in young mice while enriching Akkermansia in aged animals. Our findings unveil an epigenetic-metabolic-microbial axis centered on Tet2-mediated regulation of bile acid metabolism, providing new insights into how host epigenetic factors shape the gut microbial ecosystem.

2026-01-13 | GSE307332 | GEO

Ceramide regulated intracellular FGF13 impairs adipose nutrient sensing and glucose metabolism

Project description:Although, ectopic ceramide accumulation impairs nutrient sensing in adipocytes, leading to deterioration in energy and glucose homeostasis, the underlying mechanisms remain poorly defined. Using, comparative screen to identify ceramide regulated effector molecule in adipose tissue, we found fibroblast growth factor 13 (FGF13) as one of the critical ceramide-effector molecules that impair nutrient sensing in adipocytes. FGF13 is a cytosolic, non-secreted FGF belonging to a non-canonical FGF family member that comprises of FGF11-FGF14 and do not activate FGF receptors. FGF13 has been implicated in numerous physiological process such as development, cardiac arrythmias, neurological disease and cancer. We demonstrate that FGF13 expression is highly induced in adipose tissue in response to a high fat diet, and its expression is negated by pharmacological and genetic interventions that inhibit ceramide biosynthesis. Inhibition of FGF13 in adipocytes (white, brown and beige), alters adipocyte morphology, prevents the development of obesity, improves glucose homeostasis, insulin sensitivity and resolves hepatic steatosis

2024-12-12 | GSE191233 | 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