Effects of chronic stress and inulin on the colonic transcriptome of mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE344924 | GEO | 2026/08/30
REPOSITORIES: GEO
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Project description:Effects of chronic stress and inulin on the colonic transcriptome of mice
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Project description:Excessive consumption of fructose leads to various cardiometabolic diseases. However, inulin, dietary fiber composed of numerous fructose molecules, exerts health-beneficial effects. Here we report that inulin shifts fructose catabolism from the host organs to gut microbiome, reversing fructose-induced hyperlipidemia, hepatic steatosis and systemic glucose intolerance. Both simultaneous and delayed inulin intake enhances fructose clearance by the small intestinal microbiome, effectively reducing fructose dose reaching the liver and colon and thus suppressing hepatic lipogenesis. Inulin also activates the hepatic de novo serine synthesis pathway and cystine uptake to augment glutathione production and reduce oxidative stress. This dual effect of inulin is blocked by antibiotics and transmittable by fecal transplantation. Moreover, inulin-enriched Bacteroides acidifaciens is protective against HFCS-induced lipogenesis. Our data provide mechanistic insights into how fructose-polymer fiber inulin rewires gut microbial fructose catabolism and protects the host from excessive fructose exposure, paving the way to mitigate fructose-induced metabolic disease.
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2013-09-03 | E-GEOD-42768 | biostudies-arrayexpress
Project description:A striking example of the intricate interplay between diet, microbiota, and host is the effect of inulin, a dietary fiber, on the intestinal epithelium. Ingestion of inulin triggers a wide range of epithelial effects in the colon, such as enhanced proliferation, increased production of mucus and antimicrobial peptides, as well as systemic effects on host metabolism and immune function that are dependent on microbiota-derived molecules. In this study, we investigated the impact of inulin on two critical aspects of diet-microbiota-host interactions: intestinal hypoxia and the modulation of hypoxia-inducible factor (HIF)-1 signaling in intestinal epithelial cells (IECs) in mice colon. To achieve this, we employed a multilayered and multi-omics approach, including dietary interventions, in vitro analysis using intestinal organoids, and both genetic and pharmacological interventions. We found that inulin intake enhances intestinal hypoxia, resulting in the stabilization of HIF-1 in IECs, an effect that is both microbiota- and host-dependent. Our study revealed that HIF-1 plays a key role in regulating IEC proliferation and intestinal stem cell (ISC) function. These changes are associated with HIF-1-dependent metabolic alterations in IECs. Our findings uncover a novel mechanism by which HIF-1 acts in the colon: it acts as a molecular brake, modulating cell proliferation in a microbiota-dependent manner and through metabolic reprogramming, highlighting the complexity of the diet-microbiota-host interactions in the gut.
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Project description:This study describes differential miRNA expression in intact colon tissue during chronic SIV infection of rhesus macaques. Ten miRNAs were found to be significantly affected by infection, with 7 down-regulated and 3 up-regulated miRNAs. The expression of one upregulated miRNA was further characterized and found to be upregulated in both colonic epithelium and lamain propria cells. Further, its expression positively correlated with colonic inflammation scores and viral loads. Additional studies suggested that its expression was driven in response to oxidative stress induced double stranded DNA damage response and may play a role in chronic activation of colonic plasma cells.
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Project description:The human gut microbiota is crucial for degrading dietary fibres from the diet. However, some of these bacteria can also degrade host glycans, such as mucins, the main component of the protective gut mucus layer. Specific microbiota species and mucin degradation patterns are associated with inflammatory processes in the colon. Yet, it remains unclear how the utilization of mucin glycans affects the degradation of dietary fibres by the human microbiota. Here, we used three dietary fibres (apple pectin, β-glucan and xylan) to study in vitro the dynamics of colon mucin and dietary fibre degradation by the human faecal microbiota. The dietary fibres showed clearly distinguishing modulatory effects on faecal microbiota composition. The utilization of colon mucin in cultures led to alterations in microbiota composition and metabolites. Metaproteome analysis showed the central role of the Bacteroides in degradation of complex fibres while Akkermansia muciniphila was the main degrader of colonic mucin. This work demonstrates the intricacy of complex glycan metabolism by the gut microbiota and how the utilization of host glycans leads to alterations in the metabolism of dietary fibres. Metaproteomics analysis of this data reveals the functional activities of the bacteria in consortia, by this contributing to a better understanding of the complex metabolic pathways within the human microbiota that can be manipulated to maximise beneficial microbiota-host interactions. In this study two different mucin samples were used: commercial porcine gastric mucin and in house prepared porcine colonic mucin. This dataset analyses the proteome of: A) autoclaved porcine colonic mucin; B) not autoclaved porcine colonic mucin; C) porcine gastric mucin.
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Project description:Roseburia inulinivorans is a recently identified motile representative of the Firmicutes that contributes to butyrate formation from a variety of dietary polysaccharide substrates in the human large intestine. Microarray analysis was used here to investigate substrate-driven gene expression changes in R. inulinivorans A2-194. A cluster of fructo-oligosaccharide (FOS)/inulin utilisation genes induced during growth on inulin included one encoding a b-fructofuranosidase protein that was prominent in the proteome of inulin-grown cells. This cluster also included a 6-phosphofructokinase and an ABC transport system, while a distinct inulin-induced 1-phosphofructokinase was linked to a fructose-specific phosphoenolpyruvate-dependent sugar phosphotransferase system (PTS II transport enzyme). Real-time PCR analysis demonstrated that the b-fructofuranosidase and adjacent ABC transport protein showed greatest induction during growth on inulin, whereas the 1-phosphofructokinase enzyme and linked PTS II transport system were most strongly up-regulated during growth on fructose, indicating that these two clusters play distinct roles in the utilization of inulin. The R. inulinivorans B-fructofuranosidase was over-expressed in E. coli and shown to hydrolyse fructans ranging from inulin down to sucrose, with greatest activity on fructo-oligosacharides. Genes induced on starch included the major extra-cellular a-amylase and two distinct a-glucanotransferases together with a gene encoding a flagellin protein. The latter response may be concerned with improving bacterial access to insoluble starch particles.
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