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Oyster mushroom against hepatic steatosis in obese Zucker rats

ABSTRACT: Hepatic steatosis is a very common response to liver injury and often attributed to metabolic disorders. Prior studies have demonstrated the efficacy of a biotechnologically produced oyster mushroom (Pleurotus sajor-caju, PSC) in alleviating hepatic steatosis in obese Zucker rats. This study aims to elucidate molecular events underlying the anti-steatotic effects of PSC.

INSTRUMENT(S): Orbitrap Eclipse

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Hepatocyte, Liver

DISEASE(S): Obesity

SUBMITTER: Günter Lochnit

LAB HEAD: Günter Lochnit

PROVIDER: PXD022905 | Pride | 2021-07-27

REPOSITORIES: Pride

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			Action	DRS
	20200318_RatLiver_highpHfrac_TMT10.msf	Msf
	20200318_RatLiver_highpHfrac_TMT1001.raw	Raw
	20200318_RatLiver_highpHfrac_TMT1002.raw	Raw
	20200318_RatLiver_highpHfrac_TMT1003.raw	Raw
	20200318_RatLiver_highpHfrac_TMT1004.raw	Raw

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Publications

Tandem mass tag-based proteomics for studying the effects of a biotechnologically produced oyster mushroom against hepatic steatosis in obese Zucker rats.

Maheshwari Garima G Wen Gaiping G Gessner Denise K DK Ringseis Robert R Lochnit Günter G Eder Klaus K Zorn Holger H Timm Thomas T

Journal of proteomics 20210504

Hepatic steatosis is a very common response to liver injury and often attributed to metabolic disorders. Prior studies have demonstrated the efficacy of a biotechnologically produced oyster mushroom (Pleurotus sajor-caju, PSC) in alleviating hepatic steatosis in obese Zucker rats. This study aims to elucidate molecular events underlying the anti-steatotic effects of PSC. Tandem mass tag (TMT) peptide labeling coupled with LC-MS/MS/MS was used to quantify and compare proteins in the livers of lea ...[more]

PMID: 33957313

Similar Datasets

Evaluation of the physiological effects of a biotechnologically produced oyster mushroom in the liver of obese Zucker rats by transcriptomics

Project description:The hypothesis was tested that biotechnologically produced Pleurotus sajor-caju (PSC) influences metabolic health of obese Zucker rats. To test this, obese Zucker rats were randomly assigned to 2 groups of 12 rats each with similar body weights (BW) and fed diets either without (OC) or with 5 % PSC (OPSC) for 4 weeks and hepatic transcript profiling was performed. Transcriptomics of the liver revealed a total of 580 transcripts differentially expressed between OPSC and OC.

2020-06-06 | GSE151882 | GEO

Treatment with ginseng flower buds extract prevents hepatic steatosis by ameliorating hepatic inflammation and insulin resistance

Project description:Background: Ginseng flower bud (GFB) is a part of ginseng with high content of ginsenosides, the known active components of ginseng. While the scientific data for the pharmacological activity of ginseng roots are accumulating, the therapeutic potential of GFB have been neglected. The current study aimed to examine the therapeutic effect of GFB on hepatic steatosis and to elucidate the underlying mechanisms. Methods: HepG2 cells treated with free fatty acids mixture and hepatocytes isolated from rats after 3 weeks of HFD feeding were used as in vitro models of hepatic steatosis for evaluation of anti-steatotic effect of GFB. The effect of GFB was further investigated in pathological conditions of hepatic steatosis induced by 12 weeks of HFD feeding in C57BL/6J mice. We performed systematical analyses on hepatic gene expression profiles in GFB treated mice. The effect of GFB on the expression profile of selected genes was validated by quantitative PCR. Results: GFB treatment markedly reduced oil red O stained lipid droplets and intracellular triglyceride levels in HepG2 cells and rat hepatocytes. In HFD-fed mice, GFB (500 mg/kg) treatment markedly reduced histological signs of hepatic steatosis and decreased hepatic triglyceride content by 34.1% compared to those of HFD. These changes by GFB treatment were accompanied by improved insulin signaling. Global gene expression analysis revealed that hepatic gene expression in the steatotic liver was reversed by GFB treatment, and the GFB-regulated genes are involved in immune process, insulin response and lipid storage. Conclusion: These findings provide a substantial evidence for the medicinal use of GFB in prevention or treatment of NAFLD through suppression of hepatic inflammation and fatty acid uptake while sensitizing hepatic insulin signaling

2021-01-01 | GSE142059 | GEO

CPEB4 prevents hepatic steatosis

Project description:CPEB4 prevents hepatic steatosis

| PRJNA322835 | ENA

Gene expression induced by blue light stimulation to oyster mushroom mycelia

Project description:Photoresponse mechanism of oyster muchroom mycelia was studied using a custom microarray prepared on the basis of the genome information (Pleurotus ostreatus PC15 v2.0) in JGI Genome Portal. Blue light stimulation to the mycelia caused the up-regulation and down-regulation of genes expression. Particulary, the genes coding rate-controlling enzymes in glycolysis, pentose phosphate, and sikimic acid pathways were up-regulated to accumulate shikimic acid dramatically.

2017-02-09 | GSE58522 | GEO

Critical Roles of the Histone Methyltransferase MLL4/KMT2D in Murine Hepatic Steatosis Directed by ABL1 and PPARγ2

Project description:The pathophysiologic continuum of non-alcoholic fatty liver disease begins with steatosis. Despite great progress in understanding the gene regulatory program directing steatosis, how it is orchestrated epigenetically is unclear. Here we show that the histone H3-lysine-4-methyltransferase, MLL4/KMT2D, plays critical roles in overnutrition-induced murine steatosis via dual mechanisms. First, in response to high fat diet (HFD), MLL4 activates the expression of PPARγ2, an overnutrition-induced steatotic transcription factor. Second, HFD enables the coactivator function of MLL4 for PPARγ2, as overnutrition-activated ABL1 kinase phosphorylates PPARγ2 and enhances its association with MLL4, facilitating recruitment of MLL4 to steatotic target genes of PPARγ2, including the PPARγ2-encoding gene itself, and their transactivation via H3-lysine-4-methylation. Consistently, inhibition of ABL1 improves the fatty liver condition of ob/ob mice by suppressing the pro-steatotic action of MLL4. Our results uncover a critical regulatory axis in overnutrition-directed steatosis, and present this ABL1-PPARγ2-MLL4 axis as a new target for anti-steatosis drug development.

2017-07-01 | GSE83940 | GEO

Diminazene aceturate (DIZE) stabilizes atherosclerotic plaques and attenuates hepatic steatosis in apolipoprotein E knockout mice by influencing macrophages polarization and taurine biosynthesis

Project description:Atherosclerosis and nonalcoholic fatty liver disease (NAFLD) are leading causes of morbidity and mortality in the Western countries. NAFLD is an important independent risk factor for the development of atherosclerosis. The renin-angiotensin system (RAS) with its two main opposing effectors: angiotensin II (Ang II) and Ang-(1-7) is widely recognized as a major regulator of cardiovascular function and body metabolic processes. Angiotensin-converting enzyme 2 (ACE2) by breaking-down Ang II forms Ang-(1-7) and thus favors Ang-(1-7) actions. Therefore, the aim of our study was to comprehensively evaluate the influence of prolonged treatment with ACE2 activator – diminazene aceturate (DIZE) on the development of atherosclerotic lesions and hepatic steatosis in apoE-/- mice fed a high-fat diet (HFD). We have shown that DIZE at a dose of 30 mg/kg/day given orally for 16 weeks was able to stabilize atherosclerotic lesions and attenuate hepatic steatosis in apoE-/- mice fed an HFD. Such effects were associated with decreased total macrophages content and increased α-smooth muscle actin levels in atherosclerotic plaques. Moreover, DIZE changed polarization of macrophages towards increased amount of anti-inflammatory M2 macrophages in atherosclerotic lesions. Interestingly, the anti-steatotic action of DIZE in the liver was related to the elevated HDL in the plasma, decreased triglycerides levels and increased biosynthesis and concentration of taurine in liver of apoE-/- mice. However, the exact molecular mechanisms of both the anti-atherosclerotic and anti-steatotic actions of DIZE require further investigations.

2021-09-09 | PXD022829 | Pride

Pleurotus ostreatus strain:baby oyster mushroom

Project description:Pleurotus ostreatus strain:baby oyster mushroom Genome sequencing

| PRJNA1098946 | ENA

Raw data for manuscript : "Serine synthesis via reversed SHMT2 activity drives glycine depletion and acetaminophen hepatotoxicity in MASLD"

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD) affects one third of the global population. Understanding metabolic pathways involved can provide insights into disease progression and treatment. Untargeted metabolomics of livers from mice with early-stage steatosis uncovered decreased methylated metabolites, suggesting altered one-carbon metabolism. The levels of glycine, a central component of one-carbon metabolism, were lower in mice with hepatic steatosis, consistent with clinical evidence. Stable-isotope tracing demonstrated that increased serine synthesis from glycine via reverse serine hydroxymethyltransferase (SHMT) is the underlying cause for decreased glycine in steatotic livers. Consequently, limited glycine availability in steatotic livers impaired glutathione synthesis under acetaminophen-induced oxidative stress, enhancing acute hepatotoxicity. Glycine supplementation or hepatocyte-specific ablation of the mitochondrial SHMT2 isoform in mice with hepatic steatosis mitigated acetaminophen-induced hepatotoxicity by supporting de novo glutathione synthesis. Thus, early metabolic changes in MASLD that limit glycine availability sensitize mice to xenobiotics even at the reversible stage of this disease.

2023-12-12 | MSV000093653 | MassIVE

RNAseq and ATACseq of oyster hepatopancreas

Project description:Hox and ParaHox genes encode transcription factors with conserved similar expression patterns in divergent animals. The Pdx (Xlox) homeobox gene, for example, is expressed in a sharp spatial domain in the endodermal cell layer of the gut in chordates, echinoderms, annelids and molluscs. The significance of comparable gene expression patterns is unclear because it is not known if downstream transcriptional targets are also conserved. We thus conducted experiments to show that a classic transcriptional target of Pdx1 in vertebrates, the insulin gene, is also a direct target of Pdx in the Pacific oyster. We report that oyster has a diversity of insulin-related genes including one co-expressed with Pdx in the endodermal layer of oyster digestive tissue. Transcriptome analysis reveals functional similarity of this tissue to vertebrate pancreas. Using ATAC-seq we identify a Pdx homeodomain binding site upstream of the endodermally-expressed oyster insulin-related gene and using cell culture demonstrate that oyster Pdx acts as a transcriptional activator through this site. These data argue that a classic homeodomain-target gene interaction dates back to the base of Bilateria.

2021-03-28 | GSE107713 | GEO

Diet steatosis in commercial crossbreed swine

Project description:This study aims to fully characterize the changes taht undergoes hepatic transcriptome due to dietically induced steatosis in commercial crossbreed pigs

2022-01-31 | GSE130924 | GEO

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