Ontology highlight
ABSTRACT:
PROVIDER: PRJNA488105 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7769060_1.fastq.gz | Fastqsanger.gz | |||
| SRR7769060_2.fastq.gz | Fastqsanger.gz | |||
| SRR7769070_1.fastq.gz | Fastqsanger.gz | |||
| SRR7769070_2.fastq.gz | Fastqsanger.gz | |||
| SRR7769080_1.fastq.gz | Fastqsanger.gz |
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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: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: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.
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Project description:Long-term dietary intake influences the structure and activity of the trillions of microorganisms residing in the human gut, but it remains unclear how rapidly and reproducibly the human gut microbiome responds to short-term macronutrient change. Here we show that the short-term consumption of diets composed entirely of animal or plant products alters microbial community structure and overwhelms inter-individual differences in microbial gene expression. The animal-based diet increased the abundance of bile-tolerant microorganisms (Alistipes, Bilophila and Bacteroides) and decreased the levels of Firmicutes that metabolize dietary plant polysaccharides (Roseburia, Eubacterium rectale and Ruminococcus bromii). Microbial activity mirrored differences between herbivorous and carnivorous mammals, reflecting trade-offs between carbohydrate and protein fermentation. Foodborne microbes from both diets transiently colonized the gut, including bacteria, fungi and even viruses. Finally, increases in the abundance and activity of Bilophila wadsworthia on the animal-based diet support a link between dietary fat, bile acids and the outgrowth of microorganisms capable of triggering inflammatory bowel disease. In concert, these results demonstrate that the gut microbiome can rapidly respond to altered diet, potentially facilitating the diversity of human dietary lifestyles. RNA-Seq analysis of the human gut microbiome during consumption of a plant- or animal-based diet.
2013-12-05 | E-GEOD-46761 | biostudies-arrayexpress
Project description:Background & Aims: The complex interactions between diet and the microbiota that influence mucosal inflammation and inflammatory bowel disease are poorly understood. Experimental colitis models provide the opportunity to control and systematically perturb diet and the microbiota in parallel to quantify the contributions between multiple dietary ingredients and the microbiota on host physiology and colitis. Methods: To examine the interplay of diet and the gut microbiota on host health and colitis, we fed over 40 different diets with varied macronutrient sources and concentrations to specific pathogen free or germ free mice either in the context of healthy, unchallenged animals or dextran sodium sulfate colitis model. Results: Diet influenced physiology in both health and colitis across all models, with the concentration of protein and psyllium fiber having the most profound effects. Increasing dietary protein elevated gut microbial density and worsened DSS colitis severity. Depleting gut microbial density by using germ-free animals or antibiotics negated the effect of a high protein diet. Psyllium fiber influenced host physiology and attenuated colitis severity through microbiota-dependent and microbiota-independent mechanisms. Combinatorial perturbations to dietary protein and psyllium fiber in parallel explain most variation in gut microbial density, intestinal permeability, and DSS colitis severity, and changes in one ingredient can be offset by changes in the other. Conclusions: Our results demonstrate the importance of examining complex mixtures of nutrients to understand the role of diet in intestinal inflammation. Keywords: IBD; Diet; Microbiota; Mouse Models; Systems Biology
2017-10-30 | GSE104461 | GEO
Project description:Polyphenols are promising therapeutics for Crohn’s disease (CD), yet their bioavailability is largely dependent on the gut microbiome. The bioactive metabolites, metabolic pathways, and anti-inflammatory mechanisms underlying their effects remain poorly defined. Through integrated multi-omics and dietary analysis, we identified hippuric acid as a reduced metabolite in CD patients and a biomarker of polyphenol–microbiome interactions. We further demonstrate that hydrocinnamic acid, derived from microbiome metabolism of dietary trans-cinnamic acid and subsequently converted to hippuric acid by the host, ameliorates colitis in mice via the PPAR-γ pathway. Notably, we identified Bifidobacterium breve Bbr60 and Escherichia coli FAH as novel hydrocinnamic acid producers, complementing the established pathway in Clostridium sporogenes and suggesting additional microbial contributors. Collectively, our findings establish hydrocinnamic acid as a diet-dependent, colon-produced, mild PPAR-γ agonist with the potential to minimize adverse effects associated with traditional PPAR-γ agonists. This work establishes a foundation for developing microbiota-targeted, polyphenol-based therapeutic strategies for CD patients.
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Project description:Prebiotic fiber bundle impact on canine gut microbiome
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Project description:<p>Findings from recent studies suggest that the community of microbes residing in the human body is important in disease etiology; however, it remains unclear whether personal factors modulate human microbial composition. Studies based on animal models indicate that differences in composition might be attributed to sex-mediated effects. We analyzed the relationship of sex, adiposity, and dietary fiber intake with gut microbial composition using fecal samples from human subjects. We explored the associations of these factors with metrics of community composition and specific taxon abundances. We found that men and women had significantly different microbial community composition and that women had reduced abundance of a major phylum. Adiposity was associated with gut microbiome composition and specifically in women but not in men. Fiber from fruits and vegetables and fiber from beans were each associated with increased abundance of specific bacterial taxa. These findings provide initial indications that sex, adiposity, and dietary fiber might play important roles in influencing the human gut microbiome. Better understanding of these factors may have significant implications for gastrointestinal health and disease prevention.</p>
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Project description:Dietary modification by consuming plant-based food with high fiber content is a primary strategy to induce weight loss in obese individuals. However, long-term usage of such fiber-enriched dieting is challenging and rapid weight regain often occurs once the high-fat dietary habit resumes. Currently, how do adipose and intestinal tissues respond to a switch between high-fiber and high-fat diet remains unknown. Here, we applied C57BL/6J mice to chow diet (CD)/high-fiber diet (HfiD)-to-high-fat diet (HFD) switching paradigms and collected mesenteric white adipose tissue (mWAT), duodenum and colon tissue sections at different time points for single-nucleus profiling and spatially resolved transcriptomic analysis, respectively. We show that the progenitors and adipocytes of HfiD-fed mWAT are more sensitive to HFD-induced molecular changes. In addition, HfiD feeding prevents the subsequent HFD-induced expansion of immune-related enterocytes in duodenum and reverses the HFD-induced enterocyte-to-goblet cell conversion in colon. Moreover, HfiD-induced microbiome changes are mostly abrogated upon HFD feeding. Our results indicate that prior HfiD feeding can alter the cellular response of adipose and intestinal tissues to subsequent HFD feeding, which highlights the impact of dietary interventions with fiber-rich food for obesity treatment from a different perspective. Our data provide a spatiotemporal resource for future hypothesis-driven studies on the mechanisms of adipose and intestinal tissue plasticity in response to diet switches.
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Project description:Dietary modification by consuming plant-based food with high fiber content is a primary strategy to induce weight loss in obese individuals. However, long-term usage of such fiber-enriched dieting is challenging and rapid weight regain often occurs once the high-fat dietary habit resumes. Currently, how do adipose and intestinal tissues respond to a switch between high-fiber and high-fat diet remains unknown. Here, we applied C57BL/6J mice to chow diet (CD)/high-fiber diet (HfiD)-to-high-fat diet (HFD) switching paradigms and collected mesenteric white adipose tissue (mWAT), duodenum and colon tissue sections at different time points for single-nucleus profiling and spatially resolved transcriptomic analysis, respectively. We show that the progenitors and adipocytes of HfiD-fed mWAT are more sensitive to HFD-induced molecular changes. In addition, HfiD feeding prevents the subsequent HFD-induced expansion of immune-related enterocytes in duodenum and reverses the HFD-induced enterocyte-to-goblet cell conversion in colon. Moreover, HfiD-induced microbiome changes are mostly abrogated upon HFD feeding. Our results indicate that prior HfiD feeding can alter the cellular response of adipose and intestinal tissues to subsequent HFD feeding, which highlights the impact of dietary interventions with fiber-rich food for obesity treatment from a different perspective. Our data provide a spatiotemporal resource for future hypothesis-driven studies on the mechanisms of adipose and intestinal tissue plasticity in response to diet switches.
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