Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1190502 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31508500_1.fastq.gz | Fastqsanger.gz | |||
| SRR31508500_2.fastq.gz | Fastqsanger.gz | |||
| SRR31508600_1.fastq.gz | Fastqsanger.gz | |||
| SRR31508600_2.fastq.gz | Fastqsanger.gz | |||
| SRR31508501_1.fastq.gz | Fastqsanger.gz |
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Project description:Dietary fiber can suppress excess adipose tissue and weight gain in rodents and humans when fed high fat diets. The gut microbiome is thought to have a key role, although exactly how remains unclear. In a tightly controlled murine study, we explored how different types of dietary fiber and doses affect the gut microbiota and gut epithelial gene expression. We show that 10% pectin and 10% FOS suppress high fat diet (HFD)-induced weight gain, effects not seen at 2% doses. Furthermore, 2 and 10% mixtures of dietary fiber were also without effect. Distinct gut microbiota profiles were stimulated at the family and operational taxonomic unit (OTU) level by the different fiber treatments. Plasma levels of the gut hormone PYY were elevated by 10% pectin and FOS, but not 10% mixed fibers, and similarly RNA seq revealed some distinct effects of the 10% single fibers on gut epithelial gene expression. These data show how the ability of dietary fiber to suppress HFD-induced weight gain is dependent upon both fiber type and dose. It also shows that the microbial response to dietary fiber is distinct and that there is not a single microbial response associated with the inhibition of adiposity and weight gain. PYY seems key to the latter response, although the role of other factors such as Reg3g and CCK needs to be explored.
2025-02-05 | GSE288466 | GEO
Project description:Purpose: Although dietary cellulose is considered health promoting, there is still a lack of understanding of cellular and molecular mechanisms. The aim of this study was to shed light on possible effects of the fiber on key players in intestinal homeostasis, including intestinal epithelial cells. Method: Mice were fed a diet containing cellulose as the only source of fiber (CD, control diet) or a fiber free diet (FFD, fiber-free diet) for four weeks and then treated with dextran sulphate sodium in the drinking water for five days. To ensure that gene signatures were derived from colonic epithelial cells and not from contaminating lymphocytes, RAG1 KO mice deficient in intraepithelial lymphocytes were used. Results: The analysis of differential expressed genes of colonic epithelial cells revealed multiple effects of dietary cellulose on the transcriptional profiles. In addition, cellulose caused a distinct clustering when comparing signature genes of different epithelial cell types. Conclusion: This study demonstrated that dietary cellulose impacts transcriptional programs in colonic epithelial cells during inflammation.
2021-05-31 | GSE151136 | GEO
Project description:We sought to examine whether directly dietary fiber application to offspring could also reverse the behavioral and neurobiological deficits characteristic of MHFD offspring. RNA-sequencing (RNA-seq) on mice hippocampus were performed in order to identify the key biological processes and pathways regulated by dietary fiber.
2021-01-01 | GSE154434 | GEO
Project description:To understand how dietary fiber affects microglial transcriptome at early stage, we fed mice diets releasing different amount of fiber and profiled microglia at 3 weeks. We found that fiber significantly altered the transcriptomic signature of microglia.
2023-09-08 | GSE186210 | GEO
Project description:Despite accepted health benefits of dietary fiber, little is known about the mechanisms by which fiber deprivation impacts the gut microbiota and alters disease risk. Using a gnotobiotic model, in which mice were colonized with a synthetic human gut microbiota, we elucidated the functional interactions between dietary fiber, the gut microbiota and the colonic mucus barrier, which serves as a primary defence against pathogens. We show that during chronic or intermittent dietary fiber deficiency, the gut microbiota resorts to host-secreted mucus glycoproteins as a nutrient source, leading to erosion of the colonic mucus barrier. Dietary fiber deprivation promoted greater epithelial access and lethal colitis by the mucosal pathogen, Citrobacter rodentium, but only in the presence of a fiber-deprived microbiota that is pushed to degrade the mucus layer. Our work reveals intricate pathways linking diet, gut microbiome and intestinal barrier dysfunction, which could be exploited to improve health using dietary therapeutics. Germ-free mice (Swiss Webster) were colonized with synthetic human gut microbiota comprising of 14 species belonging to five different phyla (names of bacterial species: Bacteroides thetaiotaomicron, Bacteroides ovatus, Bacteroides caccae, Bacteroides uniformis, Barnesiella intestinihominis, Eubacterium rectale, Marvinbryantia formatexigens, Collinsella aerofaciens, Escherichia coli HS, Clostridium symbiosum, Desulfovibrio piger, Akkermansia muciniphila, Faecalibacterium prausnitzii and Roseburia intestinalis). These mice were fed either a fiber-rich diet or a fiber-free diet for about 6 weeks. The mice were then sacrificed and their cecal tissues were immediately flash frozen for RNA extraction. The extracted RNA was subjected to microarray analysis based on Mouse Gene ST 2.1 strips using the Affy Plus kit. Expression values for each gene were calculated using robust multi-array average (RMA) method.
2016-11-21 | GSE79067 | GEO
Project description:Feeding dietary fiber is known to provide us many beneficial effects. We used microarrays to detail the changes of gene expression in colons of mice fed the psyllium fiber for 5 days.
2017-05-26 | GSE99292 | GEO
Project description:Cancer cachexia and the associated skeletal muscle wasting are considered poor prognostic factors, although effective treatment has not yet been established. Recent studies have indicated that the pathogenesis of skeletal muscle loss may involve dysbiosis of the gut microbiota and the accompanying chronic inflammation or altered metabolism. In this study, we evaluated the possible effects of modifying the gut microenvironment with partially hydrolyzed guar gum (PHGG), a soluble dietary fiber, on cancer-related muscle wasting and its mechanism using a colon-26 murine cachexia model. Compared to a fiber-free (FF) diet, PHGG contained fiber-rich (FR) diet attenuated skeletal muscle loss in cachectic mice by suppressing the elevation of the major muscle-specific ubiquitin ligases Atrogin-1 and MuRF1, as well as the autophagy markers LC3 and Bnip3. Although tight junction markers were partially reduced in both FR and FF diet-fed cachectic mice, the abundance of Bifidobacterium, Akkermansia, and unclassified S24-7 family increased by FR diet, contributing to the retention of the colonic mucus layer. The reinforcement of the gut barrier function resulted in the controlled entry of pathogens into the host system and reduced circulating levels of lipopolysaccharide-binding protein (LBP) and IL-6, which in turn led to the suppression of proteolysis by downregulating the ubiquitin-proteasome system and autophagy pathway. These results suggest that dietary fiber may have the potential to alleviate skeletal muscle loss in cancer cachexia, providing new insights for developing effective strategies in the future.
2021-11-23 | E-MTAB-11094 | biostudies-arrayexpress
Project description:Interventions: Experimental group:Dietary fiber;Control:Non-Dietary fiber
Primary outcome(s): Hgb, ALB, PAB, TRF, LYM, CD3+, CD3+CD4+, CD3+CD8+, CD16+CD56+, CD19+, IgA, IgG, IgM;16S rRNA gene v3v4 variable region
Study Design: Randomized parallel controlled trial
| 2666161 | ecrin-mdr-crc