FiberMix study
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB47404 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR6662820_1.fastq.gz | Fastqsanger.gz | |||
| ERR6662820_2.fastq.gz | Fastqsanger.gz | |||
| ERR6662830_1.fastq.gz | Fastqsanger.gz | |||
| ERR6662830_2.fastq.gz | Fastqsanger.gz |
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Project description:Analysis of non-differentiated Caco-2 intestinal epithelial cell line treated with polydextrose fermentation metabolites fermented for 48 hours in 4-stage in vitro colon simulator, in which the conditions mimic the human proximal, ascending, transverse and distal colon in sequence , as well as with medium, 100 mM NaCl and 5 mM butyrate. Polydextrose, a soluble fiber fermented in colon, was fermented with the in vitro colon simulator in three amounts of 0%, 1% and 2%. Results provide insight into the mechanisms underlying colon cancer cells and a comparison of a complex fiber metabolome to 5 mM butyrate and 100 mM NaCl. Furthermore, the results give insight of dosage effect of increasing the concentration of fiber. High level of dietary fiber has been epidemiologically linked to protection against the risk for developing colon cancer. The mechanisms of this protection are not clear. Fermentation of dietary fiber in the colon results in production of for example butyrate that has drawn attention as a chemopreventive agent. Polydextrose, a soluble fiber that is only partially fermented in colon, was fermented in an in vitro colon simulator, in which the conditions mimic the human proximal, ascending, transverse and distal colon in sequence. The subsequent fermentation metabolome were applied on colon cancer cells, and the gene expression changes studied. Polydextrose fermentation down-regulated classes linked with cell cycle, and affected number of metabolically active cells. Further, up-regulated effects on classes linked with apoptosis implicate that polydextrose fermentation plays a role in induction of apoptosis in colon cancer cells. The up-regulated genes involved also key regulators of lipid metabolism, such as PPARg and PGC-1α. These results offer hypotheses for the mechanisms of two health benefits linked with consumption of dietary fiber, reducing risk of development of colon cancer, and dyslipidemia. Non-differentiated Caco-2 cells were treated with polydextrose fermentation metabolites from the vessels representing different parts of the colon, or with 100 mM NaCl or with 5 mM butyrate for 24 hours. For polydextrose fermentation three concentrations of polydextrose were used: 0%, 1% and 2% for a simulation that lasted for 48 hours. Polydextrose fermentation samples from total of 12 vessels, as well as from medium sample, 5 mM butyrate and 100 mM NaCl were analysed as single replica.
2011-04-22 | E-GEOD-28792 | biostudies-arrayexpress
Project description:Analysis of non-differentiated Caco-2 intestinal epithelial cell line treated with polydextrose fermentation metabolites fermented for 48 hours in 4-stage in vitro colon simulator, in which the conditions mimic the human proximal, ascending, transverse and distal colon in sequence , as well as with medium, 100 mM NaCl and 5 mM butyrate. Polydextrose, a soluble fiber fermented in colon, was fermented with the in vitro colon simulator in three amounts of 0%, 1% and 2%. Results provide insight into the mechanisms underlying colon cancer cells and a comparison of a complex fiber metabolome to 5 mM butyrate and 100 mM NaCl. Furthermore, the results give insight of dosage effect of increasing the concentration of fiber. High level of dietary fiber has been epidemiologically linked to protection against the risk for developing colon cancer. The mechanisms of this protection are not clear. Fermentation of dietary fiber in the colon results in production of for example butyrate that has drawn attention as a chemopreventive agent. Polydextrose, a soluble fiber that is only partially fermented in colon, was fermented in an in vitro colon simulator, in which the conditions mimic the human proximal, ascending, transverse and distal colon in sequence. The subsequent fermentation metabolome were applied on colon cancer cells, and the gene expression changes studied. Polydextrose fermentation down-regulated classes linked with cell cycle, and affected number of metabolically active cells. Further, up-regulated effects on classes linked with apoptosis implicate that polydextrose fermentation plays a role in induction of apoptosis in colon cancer cells. The up-regulated genes involved also key regulators of lipid metabolism, such as PPARg and PGC-1α. These results offer hypotheses for the mechanisms of two health benefits linked with consumption of dietary fiber, reducing risk of development of colon cancer, and dyslipidemia.
2011-04-22 | GSE28792 | GEO
Project description:A diet rich in dietary fiber and polyphenols supports the normal intestinal barrier function crucial for intestinal and overall health. Birch wood-derived fiber containing glucuronoxylans (GX)- and polyphenols have the potential in multiple food technological applications and have favorable effects on gut microbiota and colonic metabolism. However, their impact on intestinal barrier function is unknown. To elucidate their potential as new intestinal health-supporting food ingredients, we investigated the effect of GX- and polyphenol-rich extract (GXpoly ) and highly purified GX-rich extract (pureGX) on the gene expression of the colon mucosa.
2023-12-01 | GSE230139 | GEO
Project description:Here we have shown that diet-mediated alterations of the gut microbiota composition cause an erosion of the colonic mucus barrier. A compensatory increase in cellular mucus production by the host is not sufficient to re-establish the barrier, possibly due to a lacking increase in mucus secretion. While microbial transplant from mice fed a fiber-rich diet can prevent the mucus defects, the mechanism seems to be independent of general fiber fermentation and rather depend on distinct bacterial species and/or their metabolites.
2017-12-22 | PXD006129 | Pride
Project description:The aim of this study was to investigate whether long term intake of pea fiber would improve colonic barrier, bacterial profile and alter colonic gene expression using DNA microarray. Fifty weaned pigs were randomly allocated into 2 groups receiving control and fibrous diet with inclusion of pea fiber from weaning age until d 160. The two diets had similar nutrient levels. Pigs fed pea fiber diet (PF diet) had markedly decreased overall average daily feed intake (ADFI) and Feed:Gain in growing and finishing period (P<0.05). In addition, long term intake of PF diet induced deeper crypt (+50 %, P<0.05), increased protein expression of colonic mucin and sIgA (+13～16 %, P<0.05). Resulting from the increased lactobacillus content (P<0.05), moreover, pigs fed PF diet had significantly higher concentration of colonic total short chain fatty acid (SCFA) and acetic acid. DNA microarray results indicated that feeding PF diet induced alterations in the expression of colonic cancer, immune response and lipid metabolism-related genes, as well as genes involved in signal pathway such as intestinal immune network for IgA production, PPAR signaling pathway and nutrient metabolism-related pathways. Collectively, our results suggested that long term intake of PF diet would improve colonic health via altering colonic bacteria profile, colonic barriers, immune and metabolism related protein or gene expressions. A total of 50 weaned pigs (Duroc×Landrace×Yorkshire, initial body weight: 7.2±0.5 kg) were randomly allocated to 2 groups with 5 pens each group and 5 pig each pen. Pigs were fed control (Control) and fibrous diets (10～20 % inclusion of pea fiber, PF) from weaning at 28 day to 160 day-old-age, which is subjected to phase feeding by weaning diet (weaning to d 30 post-weaning), growing diet (d 30～90 postweaning) and finishing diet (d 90～160 postweaning) according to their physiological stage. At d 160 postweaning, four pigs each group were selected to be slaughtered for collection of colonic tissues and DNA microarray was applied to the colonic tissues for analysis of gene expression.
2013-01-30 | E-GEOD-43917 | biostudies-arrayexpress
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:The aim of this study was to investigate whether long term intake of pea fiber would improve colonic barrier, bacterial profile and alter colonic gene expression using DNA microarray. Fifty weaned pigs were randomly allocated into 2 groups receiving control and fibrous diet with inclusion of pea fiber from weaning age until d 160. The two diets had similar nutrient levels. Pigs fed pea fiber diet (PF diet) had markedly decreased overall average daily feed intake (ADFI) and Feed:Gain in growing and finishing period (P<0.05). In addition, long term intake of PF diet induced deeper crypt (+50 %, P<0.05), increased protein expression of colonic mucin and sIgA (+13～16 %, P<0.05). Resulting from the increased lactobacillus content (P<0.05), moreover, pigs fed PF diet had significantly higher concentration of colonic total short chain fatty acid (SCFA) and acetic acid. DNA microarray results indicated that feeding PF diet induced alterations in the expression of colonic cancer, immune response and lipid metabolism-related genes, as well as genes involved in signal pathway such as intestinal immune network for IgA production, PPAR signaling pathway and nutrient metabolism-related pathways. Collectively, our results suggested that long term intake of PF diet would improve colonic health via altering colonic bacteria profile, colonic barriers, immune and metabolism related protein or gene expressions.
2013-01-30 | GSE43917 | GEO
Project description:BACKGROUND: Appendicitis followed by appendectomy (AA) at a young age protects against later inflammatory bowel disease (IBD). Using a novel murine appendicitis model we earlier demonstrated that AA proffered significant protection against subsequent experimental colitis. AIM: To delineate genes and biological pathways involved in the protective effect of AA against subsequent colitis using gene set enrichment analysis (GSEA) of DNA microarray data. METHODS: Appendicitis and appendicectomy was done (5 week old male BALB/c mice) near the most proximal colon (caecal lymphoid follicles) and colonic samples were harvested from the most distal colon. Two consecutive laparotomies were done in control Sham-Sham (SS) mice. RNA was extracted (TRIzol®) from 4 individual colonic samples per group (AA group vs. SS group) with each sample taken independently through Affymetrix® microarray hybridization. For GSEA, data for more than 23,000 genes were exported from Partek and analyzed with GSEA software (with 2852 gene sets encoded) to establish correlates with phenotypes of the gene sets. RESULTS: Distal colonic expression of 636 gene-sets were significantly upregulated in AA group samples (False Discovery Rates (FDR) values < 1 % and p value < 0.001; stringent statistical selection). These were validated by quantitative PCR of 14 selected genes across the immunological spectrum and over time-intervals of 3 days, 14 days and 28 days. CONCLUSIONS: Many key immunological, apoptosis-related and cellular function-associated gene-sets involved in the protective effect of AA in experimental colitis were identified. Further analysis of these profiles and biological pathways will assist utilizing these gene products and manipulating various aspects of these pathways to develop better therapeutic strategies in the management of intractable IBD. Appendicitis and appendicectomy was done (5 week old male BALB/c mice) near the most proximal colon (caecal lymphoid follicles) and colonic samples were harvested from the most distal colon. Two consecutive laparotomies were done in control Sham-Sham (SS) mice. RNA was extracted (TRIzol®) from 4 individual colonic samples per group (AA group vs. SS group) with each sample taken independently through Affymetrix® microarray hybridization. variable_protocol: appendicitis and appendectomy: AA1, AA2, AA3, AA4 variable_protocol: sham/sham surgery: SS1, SS2, SS3, SS4 repeat_biological replicate: AA1, AA2, AA3, AA4 repeat_biological replicate: SS1, SS2, SS3, SS4 Upregulated gene-set linked as supplementary file.
2010-09-01 | E-GEOD-23914 | biostudies-arrayexpress
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