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Imbalanced gut microbiota drives nonalcoholic fatty liver disease and nonalcoholic steatohepatitis in a fast-food diet mouse model

ABSTRACT: Imbalanced gut microbiota drives nonalcoholic fatty liver disease and nonalcoholic steatohepatitis in a fast-food diet mouse model

PROVIDER: PRJNA789248 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17261500_1.fastq.gz	Fastqsanger.gz
	SRR17261500_2.fastq.gz	Fastqsanger.gz
	SRR17261600_1.fastq.gz	Fastqsanger.gz
	SRR17261600_2.fastq.gz	Fastqsanger.gz
	SRR17261501_1.fastq.gz	Fastqsanger.gz

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Imbalanced gut microbiota drives nonalcoholic fatty liver disease and nonalcoholic steatohepatitis in a fast-food diet mouse model

Project description:This study employed low and high-fat purified diets containing two levels of added dietary cholesterol in conventionally raised, specific-pathogen free (SPF) mice harboring a full microbial community as compared to germ-free (GF) mice raised in complete absence of gut microbes on disease outcomes. It was hypothesized that FF-diets would lead to an earlier onset of gut dysbiosis, corresponding with elevated biomarkers of NAFLD and NASH. In the present study, we aimed to dissect the role of FF diet induced gut dysbiosis in order to mechanistically identify the underlying mechanism that influences gut-liver crosstalk between specific diet-induced bacterial populations and hepatic tissue to drive NAFLD/NASH onset and progression

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Imbalanced gut microbiota predicts and drives the progression of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis in a fast-food diet mouse model.

Project description:Nonalcoholic fatty liver disease (NAFLD) is multifactorial in nature, affecting over a billion people worldwide. The gut microbiome has emerged as an associative factor in NAFLD, yet mechanistic contributions are unclear. Here, we show fast food (FF) diets containing high fat, added cholesterol, and fructose/glucose drinking water differentially impact short- vs. long-term NAFLD severity and progression in conventionally-raised, but not germ-free mice. Correlation and machine learning analyses independently demonstrate FF diets induce early and specific gut microbiota changes that are predictive of NAFLD indicators, with corresponding microbial community instability relative to control-fed mice. Shotgun metagenomics showed FF diets containing high cholesterol elevate fecal pro-inflammatory effectors over time, relating to a reshaping of host hepatic metabolic and inflammatory transcriptomes. FF diet-induced gut dysbiosis precedes onset and is highly predictive of NAFLD outcomes, providing potential insights into microbially-based pathogenesis and therapeutics.HighlightsGerm-free mice are protected from fast-food diet-induced NAFLD.Fast-food diets rapidly shift gut microbiota composition and function.Increasing dietary cholesterol exacerbates hepatic inflammation only in SPF mice.Fast-food diet-induced gut dysbiosis precedes and predicts late-stage NAFLD severity.

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