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ABSTRACT: Microbial community of fecal samples in mice with chronic and and binge ethanol feeding model (the NIAAA model)

PROVIDER: PRJNA776682 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16660300_1.fastq.gz	Fastqsanger.gz
	SRR16660300_2.fastq.gz	Fastqsanger.gz
	SRR16660301_1.fastq.gz	Fastqsanger.gz
	SRR16660301_2.fastq.gz	Fastqsanger.gz
	SRR16660302_1.fastq.gz	Fastqsanger.gz

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Hepatic CYP2B10 is highly induced by binge ethanol and contributes to acute-on-chronic alcohol-induced liver injury

Project description:We altered the NIAAA (Gao Binge Model) of 8 week chronic plus binge ethanol (E8G1) to have 3 total ethanol gavages (5 g/kg; 1 every 24h) of ethanol after 8 weeks of chronic ethanol feeding (E8G3) to determine how the liver responds to chronic plus consecutive binge ethanol. Surprisingly, E8G3 treatment induced lower levels of liver injury, steatosis, inflammation, and fibrosis as compared to mice after E8G1 treatment. Microarray analyses were performed, identifying several pathways that may contribute to the observed liver adaptation to binge ethanol. In addition, cytochrome P450 2B10 (Cyp2b10) was a top upregulated gene in the E8G1 group and further upregulated in the E8G3 group, but only moderately induced after chronic ethanol consumption, which was confirmed by RT-qPCR and western blot analyses. Genetic disruption of the Cyp2b10 gene worsened liver injury in E8G1 and E8G3 mice with higher blood ethanol levels compared to wild-type control mice, while in vitro experimentation revealed that CYP2b10 did not directly promote ethanol metabolism. Metabolomic analyses revealed significant differences in hepatic metabolites from E8G1-treated Cyp2b10 KO and WT mice, and these metabolic alterations may contribute to the reduced liver injury in Cyp2b10 KO mice.

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Next-generation sequencing (NGS) facilitates quantitative analysis of differentially expressed genes in ethanol-fed murine livers after ethanol binge

Project description:Purpose: The goals of this study are to use NGS-derived liver transcriptome profiling (RNA-seq) and identify differentially expressed genes in damaged livers that were exposed to 5% ethanol-containing liquid diet and ethanol binge. Methods: Liver mRNA profiles were generated from chronic ethanol feeding plus a single binge by deep sequencing, in duplicate, using Illumina Hiseq2500. qRT–PCR validation was performed using SYBR Green assay. Results: Chronic ethanol feeding plus a single binge treatment was associated with 422 downregulated genes and 384 upregulated genes, whereas Yap1 null livers had 351 downregulated genes and 287 upregulated genes after ethanol/CCl4 induced liver damage. Conclusions: This study provides detailed analysis of liver transcriptomes during hepatocyte damage caused by chronic ethanol feeding plus a single binge treatment, with biologic replicates, generated by RNA-seq technology.

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Fat-specific protein 27/CIDEC plays an important role in promoting alcoholic liver injury in mice and humans

Project description:Here, we developed a mouse model with long-term chronic (8-12 week) plus single/multiple binge ethanol feeding, which mimicks the drinking patterns of AH patients, who often have a history of chronic drinking plus recent excessive drinking. This model produces severe macrosteatosis, significant inflammation, and mild fibrosis. Moreover, we conducted translational studies by comparing transcriptome data from this clinically relevant in vivo model and human AH biopsy samples, and identified many similar disregulated genes in this animal model and AH samples. And we find that FSP27/CIDE-C plays a critical role in promoting steatosis and hepatocellular damage in mouse and in human AH.

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A novel model of binge ethanol exposure reveals enhanced neurodegeneration with advanced age

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Chronic alcohol drinking compromises lung immunity by altering immunometabolism in both human and mouse lungs

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