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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [16s rDNA-seq]

ABSTRACT: IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [16s rDNA-seq]

PROVIDER: PRJNA1015547 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26037800_1.fastq.gz	Fastqsanger.gz
	SRR26037800_2.fastq.gz	Fastqsanger.gz
	SRR26037801_1.fastq.gz	Fastqsanger.gz
	SRR26037801_2.fastq.gz	Fastqsanger.gz
	SRR26037802_1.fastq.gz	Fastqsanger.gz

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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis

Project description:IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis

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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [scRNA-seq]

Project description:IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [scRNA-seq]

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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [16s rDNA-seq]

Project description:IL22 induces antimicrobial peptides which influnce microbiota. We used 16s rRNA gene sequencing (16s DNA-seq) to analyze the microbiota with Fc or IL-22Fc treatment.

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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis

Project description:This SuperSeries is composed of the SubSeries listed below.

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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [scRNA-seq]

Project description:We found IL22 could reduce intestinal fatty acid transporters expression. We used single cell RNA sequencing (scRNA-seq) to analyze the cell population and gene expression with Fc or IL-22Fc treatment.

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Intestinal organoid expression data from patients with MASLD-cirrhosis versus non-fibrotic MASLD

Project description:This study aimed to establish and characterize an in vitro model of human intestinal organoids isolated from duodenal samples of patients with non-fibrotic MASLD and those with MASLD-cirrhosis. Whole transcriptome analysis and the energetic and redox status of the organoids were assessed to characterize intestinal functional impairment in the context of MASLD. We used microarrays to detail the whole transcriptome dysregulation underlying intestinal dysfunction in organoids isolated from chirrotic versus non-fibrotic MASLD patients.

2025-09-04 | GSE299719 | GEO

Allantoin promotes MASLD progression

Project description:Uric acid has garnered increasing attention for its association with metabolic dysfunction-associated steatotic liver disease (MASLD) in recent cross-sectional studies, although detailed understanding of its involvement remains limited. This study confirms a strong association between urate levels and elevated risk of both MASLD and type 2 diabetes (T2D) through a large-scale observational analysis of UK Biobank data. However, Mendelian randomization (MR) analysis involving over 2 million samples identified only causal effects of urate on serum triglyceride levels and the risk of T2D. Additionally, a targeted metabolomics study involving elderly Chinese participants revealed that, rather than UA, allantoin—a byproduct of UA oxidation—was significantly elevated in individuals with dyslipidemia or T2D. Notably, a significant negative correlation was found between serum allantoin level and fasting glucose, as well as serum triglyceride and cholesterol levels. Animal studies demonstrated that allantoin exacerbates hepatic lipid accumulation and glucose intolerance in mice fed a high-fat diet, which was accompanied by increased hepatic lipid biogenesis and reduced bile acid production. Interestingly, our findings indicate that allantoin exhibits a strong binding affinity for PPARα, suggesting that it may act as an inhibitor of PPARα, thereby promoting the progression of MASLD. These results underscore the critical role of allantoin, rather than UA, in the development of MASLD, offering valuable insights for the prediction and management of hepatic metabolic disorders.

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Allantoin promotes MASLD progression

Project description:Allantoin promotes MASLD progression

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Effect of hepatocytic RKIP depletion on HFD-induced MASLD

Project description:High-fat diet (HFD) is a risk factor for metabolic dysfunction-associated steatotic liver disease (MASLD), yet the molecular pathways that connect dietary fats to liver dysfunction remain unclear. Hepatocyte-specific RKIP depletion in male mice exacerbates ER stress, resulting in lipid droplets accumulation and MASLD progression.

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Project description:The burden of senescent hepatocytes correlates with MASLD severity but mechanisms driving senescence, and how it exacerbates MASLD are poorly understood. Hepatocytes become senescent when Smoothened (Smo) is deleted to disrupt Hedgehog signaling. We aimed to determine if the secretomes of Smo-deficient hepatocytes perpetuate senescence to drive MASLD progression. RNA seq analysis confirmed that hepatocyte populations of MASLD livers are depleted of Smo(+) cells and enriched with senescent cells. When fed CDA-HFD, Smo(-) mice had lower antioxidant markers and developed worse DNA damage, senescence, MASH and liver fibrosis than Smo(+) mice. Sera and hepatocyte-conditioned medium from Smo(-) mice were depleted of thymidine phosphorylase (TP), a protein that maintains mitochondrial fitness. Treating Smo(-) hepatocytes with TP reduced senescence and lipotoxicity; inhibiting TP in Smo(+) hepatocytes had the opposite effects and exacerbated hepatocyte senescence, MASH, and fibrosis in CDA-HFD-fed mice.Therefore, we found that inhibiting Hedgehog signaling in hepatocytes promotes MASLD by suppressing hepatocyte production of proteins that prevent lipotoxicity and senescence.

2024-10-01 | GSE273523 | GEO

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