RNA sequencing(RNA-Seq)in liver tissues from different exercise interventions in NAFLD mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1209934 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31980428_1.fastq.gz | Fastqsanger.gz | |||
| SRR31980428_2.fastq.gz | Fastqsanger.gz | |||
| SRR31980429_1.fastq.gz | Fastqsanger.gz | |||
| SRR31980429_2.fastq.gz | Fastqsanger.gz | |||
| SRR31980430_1.fastq.gz | Fastqsanger.gz |
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Project description:RNA sequencing(RNA-Seq)in liver tissues from different exercise interventions in NAFLD mice
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Project description:Cysteine dioxygenase type 1 (Cdo1) is a key enzyme for cysteine catabolism that is enriched in liver, whose role in NAFLD remains poorly understood. Here, we show that exercise induces the expression of hepatic Cdo1 via the cAMP/PKA/CREB signaling pathway. Hepatocyte-specific knockout of Cdo1 (Cdo1LKO) impairs the effect of exercise against NAFLD, whereas hepatocyte-specific overexpression of Cdo1 (Cdo1LTG) and exercise synergistically ameliorates NAFLD in male mice. Mechanistically, Cdo1 facilitates the binding between AMPK and kinase active Camkk2, which activates AMPK signaling. This promotes fatty acid oxidation and mitochondrial biogenesis in hepatocytes to attenuate hepatosteatosis. Therefore, by promoting hepatic Camkk2-AMPK signaling pathway, Cdo1 acts as an important downstream effector of exercise to combat against NAFLD
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Project description:Lean nonalcoholic fatty liver disease (NAFLD) is increasingly recognized as a distinct clinical phenotype with limited evidence for effective non-pharmacological interventions and unclear mechanistic pathways. Aerobic exercise is recommended for NAFLD management, yet its effects and underlying gut microbiota–mediated mechanisms in lean NAFLD remain insufficiently characterized. This study is based on a randomized controlled trial (ClinicalTrials.gov identifier: NCT04882644) in which 100 adults with lean NAFLD were randomly assigned to a 3-month aerobic exercise intervention or usual care. 63 paired fecal samples were collected at baseline and after intervention. Gut microbiota profiles were generated using 16S rRNA gene sequencing. The dataset includes processed taxonomic abundance tables derived from fecal samples collected before and after the intervention. These data were used to characterize exercise-induced alterations in gut microbial diversity, composition, and functional potential, and to explore interindividual heterogeneity in microbiota responses to aerobic exercise in lean NAFLD. The microbiome data deposited in this series support integrative analyses with clinical phenotypes and circulating metabolomic profiles, aiming to elucidate gut microbiota–associated mechanisms underlying the metabolic benefits of aerobic exercise in lean NAFLD.
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Project description:Lean nonalcoholic fatty liver disease (NAFLD) is increasingly recognized as a distinct clinical phenotype with limited evidence for effective non-pharmacological interventions and unclear mechanistic pathways. Aerobic exercise is recommended for NAFLD management; however, its effects and the gut microbiota–associated mechanisms in lean NAFLD remain incompletely understood. This dataset was generated from a randomized controlled trial (ClinicalTrials.gov identifier: NCT04882644). Participants assigned to the aerobic exercise intervention group provided fecal samples at baseline and after the 3-month intervention. A total of 33 paired fecal samples were included in this dataset. Gut microbiota profiles were generated using shotgun metagenomic sequencing. The dataset includes processed and de-identified species-level relative abundance tables derived from fecal samples collected before and after the intervention. These data were used to characterize exercise-induced alterations in gut microbial composition and interindividual variability in microbiota responses to aerobic exercise in lean NAFLD. The data support integrative analyses with clinical phenotypes and circulating metabolomic profiles to explore gut microbiota–associated mechanisms underlying the metabolic benefits of aerobic exercise.
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Project description:Non-alcoholic fatty liver disease (NAFLD) is associated with obesity and lifestyle. Exercise is known to be beneficial for NAFLD treatment. Recent studies have shown the critical involvement of microRNA in NAFLD. However, it is unclear whether exercise could prevent NAFLD via miRNA targeting. We used microarrays to examine microRNA profiles in high-fat diet fed mice with and without exercise in comparison to normal diet fed mice.
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Project description:We studied the opposing effects of exercise training and high-fat diet at single-cell resolution to reveal changes in cell type abundance, cell-type-specific gene expression/pathway/regulatory network changes, and changes in cell-cell communication both within and across tissues. We profiled scRNA-seq in 204,883 cells, grouped into 53 distinct cell sub-types/states across 22 major cell types, from subcutaneous white adipose tissue, visceral white adipose tissue, and skeletal muscle across 16 lean and 15 obese mice with both diet and exercise interventions. Changes in both cell proportion and transcriptional state were most strongly pronounced in adipose stem cells in fat, consistent with roles of adipogenesis in thermogenesis-vs-lipogenesis and hyperplasia-vs-hypertrophy in obesity. For immune cells, exercise training decreases obesity-associated inflammatory tissue-resident cell populations, including myeloid and regulatory T cells, and promotes beige-cell-inducing populations, including NKT cells. These changes clustered in common pathways across tissues for both exercise and obesity, including extracellular matrix remodelling and circadian rhythm in mesenchymal stem cells and cell activation/migration in immune cells.
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