Mouse gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA604973 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11035700_1.fastq.gz | Fastqsanger.gz | |||
| SRR11035700_2.fastq.gz | Fastqsanger.gz | |||
| SRR11035701_1.fastq.gz | Fastqsanger.gz | |||
| SRR11035701_2.fastq.gz | Fastqsanger.gz | |||
| SRR11035702_1.fastq.gz | Fastqsanger.gz |
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Project description:Gut microbiome research is rapidly moving towards the functional characterization of the microbiota by means of shotgun meta-omics. Here, we selected a cohort of healthy subjects from an indigenous and monitored Sardinian population to analyze their gut microbiota using both shotgun metagenomics and shotgun metaproteomics. We found a considerable divergence between genetic potential and functional activity of the human healthy gut microbiota, in spite of a quite comparable taxonomic structure revealed by the two approaches. Investigation of inter-individual variability of taxonomic features revealed Bacteroides and Akkermansia as remarkably conserved and variable in abundance within the population, respectively. Firmicutes-driven butyrogenesis (mainly due to Faecalibacterium spp.) was shown to be the functional activity with the higher expression rate and the lower inter-individual variability in the study cohort, highlighting the key importance of the biosynthesis of this microbial by-product for the gut homeostasis. The taxon-specific contribution to functional activities and metabolic tasks was also examined, giving insights into the peculiar role of several gut microbiota members in carbohydrate metabolism (including polysaccharide degradation, glycan transport, glycolysis and short-chain fatty acid production). In conclusion, our results provide useful indications regarding the main functions actively exerted by the gut microbiota members of a healthy human cohort, and support metaproteomics as a valuable approach to investigate the functional role of the gut microbiota in health and disease.
2017-07-19 | PXD005780 | Pride
Project description:Our preliminary data suggest that PPA, a gut microbiota derived metabolite, reduced APAP hepatotoxicity. The goal of our study is to determine whether PPA modulates hepatic gene expressions and thus modulate APAP hepatotoxicity.
2026-01-25 | GSE144860 | GEO
Project description:The effect of 3-phenylpropionic acid (PPA) on hepatic gene expressions
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Project description:We have previously demonstrated that the gut microbiota can play a role in the pathogenesis of conditions associated with exposure to environmental pollutants. It is well accepted that diets high in fermentable fibers such as inulin can beneficially modulate the gut microbiota and lessen the severity of pro-inflammatory diseases. Therefore, we aimed to test the hypothesis that hyperlipidemic mice fed a diet enriched with inulin would be protected from the pro-inflammatory toxic effects of PCB 126.
2020-02-27 | E-MTAB-8798 | biostudies-arrayexpress
Project description:<p>Cold exposure induces beige adipogenesis in white adipose tissue (iWAT), enhancing thermogenesis and energy expenditure. While gut microbiota-derived metabolites are known to regulate host metabolism, their role in thermogenic adaptation remains poorly defined. Here, we identify Prevotella copri (P. copri) as a key microbial mediator of cold-induced adipose remodeling. Cold exposure expands the population of P. copri in the colonic contents, and we found that this species that produces 3-phenylpropionic acid (3-PPA) to promote beige adipocyte formation and enhances energy expenditure. Mechanistically, 3-PPA signals through free fatty acid receptor 1 (Ffar1/Gpr40) in M2-like macrophages, inducing C-X-C motif chemokine 13 (CXCL13) secretion that in turn recruits T follicular helper (Tfh) cells to facilitate beige adipogenesis. By lineage-tracing analyses, we reveal that adipocyte progenitor cells contribute to 3-PPA-driven beige fat formation. Moreover, 3-PPA supplementation counteracts high-fat diet–induced obesity in mice and promotes thermogenesis in mouse, pig, and human adipose progenitor cells. These findings define a gut microbiota–immune cell-adipose progenitor cell axis that regulates cold adaptation, highlighting microbial metabolites as potential therapeutic targets for metabolic diseases.</p>
2025-12-13 | MTBLS13503 | MetaboLights
Project description:Effect of HGF on gut microbiota in mice with periodontitis
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Project description:Mardinoglu2015 - Generic mouse genome-scale
metabolic network (MMR)
This model is described in the article:
The gut microbiota modulates
host amino acid and glutathione metabolism in mice.
Mardinoglu A, Shoaie S, Bergentall
M, Ghaffari P, Zhang C, Larsson E, Bäckhed F, Nielsen
J.
Mol. Syst. Biol. 2015; 11(10):
834
Abstract:
The gut microbiota has been proposed as an environmental
factor that promotes the progression of metabolic diseases.
Here, we investigated how the gut microbiota modulates the
global metabolic differences in duodenum, jejunum, ileum,
colon, liver, and two white adipose tissue depots obtained from
conventionally raised (CONV-R) and germ-free (GF) mice using
gene expression data and tissue-specific genome-scale metabolic
models (GEMs). We created a generic mouse metabolic reaction
(MMR) GEM, reconstructed 28 tissue-specific GEMs based on
proteomics data, and manually curated GEMs for small intestine,
colon, liver, and adipose tissues. We used these functional
models to determine the global metabolic differences between
CONV-R and GF mice. Based on gene expression data, we found
that the gut microbiota affects the host amino acid (AA)
metabolism, which leads to modifications in glutathione
metabolism. To validate our predictions, we measured the level
of AAs and N-acetylated AAs in the hepatic portal vein of
CONV-R and GF mice. Finally, we simulated the metabolic
differences between the small intestine of the CONV-R and GF
mice accounting for the content of the diet and relative gene
expression differences. Our analyses revealed that the gut
microbiota influences host amino acid and glutathione
metabolism in mice.
This model is hosted on
BioModels Database
and identified by:
MODEL1509220028.
To cite BioModels Database, please use:
BioModels Database:
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quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2015-11-04 | MODEL1509220028 | BioModels
Project description:Approximately 15% of US adults have circulating levels of uric acid above its solubility limit, which is causally linked to the inflammatory disease gout. In most mammals, uric acid elimination is facilitated by the enzyme uricase. However, human uricase is a pseudogene, having been inactivated early in hominid evolution. Though it has long been known that a substantial amount of uric acid is eliminated in the gut, the role of the gut microbiota in hyperuricemia has not been studied. Here we identify a gene cluster, widely distributed in the gut microbiome, that encodes a pathway for uric acid degradation. Stable isotope tracing demonstrates that gut bacteria metabolize uric acid to xanthine or short chain fatty acids such as acetate, lactate and butyrate. Ablation of the microbiota in uricase-deficient mice causes profound hyperuricemia, and anaerobe-targeted antibiotics increase the risk of gout in humans. These data reveal a role for the gut microbiota in uric acid excretion and highlight the potential for microbiome-targeted therapeutics in hyperuricemia.
2023-06-16 | GSE206419 | GEO
Project description:Background: The long-term high-fat, high-sugar diet exacerbates type 2 diabetes mellitus (T2DM)-related cognitive impairments. The negative impact of poor dietary patterns on brain development and neurological function may be related to gut microbiota disturbance. The role of phlorizin in mitigating glucose and lipid metabolism disorders is well documented. However, the protective effect of phlorizin on diabetes-related cognitive dysfunction is unclear. Therefore, the present study aimed to investigate the effect of dietary supplementation of phlorizin on high-fat and high-fructose diet (HFFD)-induced cognitive dysfunction and evaluate the crucial role of the microbiota-gut-brain axis. Results: Dietary supplementation of phlorizin for 14 weeks effectively prevented glucolipid metabolism disorder, spatial learning impairment, and memory impairment in HFFD mice. In addition, phlorizin improved the HFFD-induced decrease in synaptic plasticity, neuroinflammation, and excessive activation of microglia in the hippocampus. Transcriptomics analysis shows that the protective effect of phlorizin on cognitive impairment was associated with increased expression of neurotransmitters and synapse-related genes in the hippocampus. Phlorizin treatment alleviated colon microbiota disturbance, mainly manifested by an increase in gut microbiota diversity and the abundance of short-chain fatty acid (SCFA)-producing bacteria. The level of microbial metabolites, including SCFA, inosine 5'-monophosphate (IMP), and D (-)-beta-hydroxybutyric acid (BHB) were also significantly increased after phlorizin treatment. Moreover, integrating multiomics analysis observed tight connections between phlorizin-regulated genes, microbiota, and metabolites. Furthermore, removal of the gut microbiota via antibiotics treatment diminished the protective effect of phlorizin against HFFD-induced cognitive impairment, underscoring the critical role of the gut microbiota in mediating cognitive behavior. Importantly, supplementation with SCFA and BHB alone mimicked the regulatory effects of phlorizin on cognitive function. Conclusions: These results indicate that gut microbiota and their metabolites mediate the ameliorative effect of phlorizin on HFFD-induced cognitive impairment. Therefore, phlorizin can be used as an easy-to-implement nutritional therapy to prevent and alleviate metabolism-related neurodegenerative diseases by targeting the regulation of the microbiome-gut-brain axis.
2024-03-20 | GSE261887 | GEO
Project description:The effect of oral microbiota on the intestinal microbiota has garnered growing attention as a mechanism linking periodontal diseases to systemic diseases. However, the salivary microbiota is diverse and comprises numerous bacteria with a largely similar composition in healthy individuals and periodontitis patients. Thus, the systemic effects of small differences in the oral microbiota are unclear. In this study, we explored how health-associated and periodontitis-associated salivary microbiota differently colonized the intestine and their subsequent systemic effects by analyzing the hepatic gene expression and serum metabolomic profiles. The salivary microbiota was collected from a healthy individual and a periodontitis patient and gavaged into C57BL/6NJcl[GF] mice. Samples were collected five weeks after administration. Gut microbial communities were analyzed by 16S ribosomal RNA gene sequencing. Hepatic gene expression profiles were analyzed using a DNA microarray and quantitative polymerase chain reaction. Serum metabolites were analyzed by capillary electrophoresis time-of-flight mass spectrometry. The gut microbial composition at the genus level was significantly different between periodontitis-associated microbiota-administered (PAO) and health-associated oral microbiota-administered (HAO) mice. The hepatic gene expression profile demonstrated a distinct pattern between the two groups, with higher expression of Neat1, Mt1, Mt2, and Spindlin1, which are involved in lipid and glucose metabolism. Disease-associated metabolites such as 2-hydroxyisobutyric acid and hydroxybenzoic acid were elevated in PAO mice. These metabolites were significantly correlated with Bifidobacterium, Atomobium, Campylobacter, and Haemophilus, which are characteristic taxa in PAO mice. Conversely, health-associated oral microbiota were associated with higher levels of beneficial serum metabolites in HAO mice. The multi-omics approach used in this study revealed that periodontitis-associated oral microbiota is associated with the induction of disease phenotype when they colonized the gut of germ-free mice.
2022-08-17 | GSE198570 | GEO