Mouse gut metagenome
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR127904_1.fastq.gz | Fastqsanger.gz | |||
| DRR127904_2.fastq.gz | Fastqsanger.gz | |||
| DRR127905_1.fastq.gz | Fastqsanger.gz | |||
| DRR127905_2.fastq.gz | Fastqsanger.gz | |||
| DRR127906_1.fastq.gz | Fastqsanger.gz |
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Project description:Aggregatibacter actinomycetemcomitans, gut microbiota in mice eating high fat diet
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Project description:Increasing the consumption of dietary fibre has been proposed to alleviate the progression of non-communicable diseases such as obesity, type 2 diabetes and cardiovascular disease, yet the effect of dietary fibre on host physiology remains unclear. In this study, we performed a multiple diet feeding study in C57BL/6J mice to compare high fat and high fat modified with dietary fibre diets on host physiology and gut homeostasis by combining proteomic, metagenomic, metabolomic and glycomic techniques with correlation network analysis. We observed significant changes in physiology, liver proteome, gut microbiota and SCFA production in response to high fat diet. Dietary fibre modification did not reverse these changes but was associated with specific changes in the gut microbiota, liver proteome, SCFA production and colonic mucin glycosylation. Furthermore, correlation network analysis identified gut bacterial-glycan associations.
2021-09-08 | PXD014132 | Pride
Project description:This study was performed to investigate the effect of aging and high fat diet on gut microbiota in F344 rats by the pyrosequencing method.
2018-12-18 | GSE104184 | GEO
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:We studied the effect of dietary fat type, varying in polyunsaturated/saturated fatty acid ratio's (P/S) on development of metabolic syndrome. C57Bl/6J mice were fed purified high-fat diets (45E% fat) containing palm oil (HF-PO; P/S 0.4), olive oil (HF-OO; P/S 1.1) or safflower oil (HF-SO; P/S 7.8) for 8 weeks. A low-fat palm oil diet (LF-PO; 10E% fat) was used as a reference. Additionally, we analyzed diet-induced changes in gut microbiota composition and mucosal gene expression. The HF-PO diet induced a higher body weight gain and liver triglyceride content compared to the HF-OO, HF-SO or LF-PO diet. In the intestine, the HF-PO diet reduced microbial diversity and increased the Firmicutes/Bacteroidetes ratio. Although this fits a typical obesity profile, our data clearly indicate that an overflow of the HF-PO diet to the distal intestine, rather than obesity itself, is the main trigger for these gut microbiota changes. A HF-PO diet-induced elevation of lipid metabolism-related genes in the distal small intestine confirmed the overflow of palm oil to the distal intestine. Some of these lipid metabolism-related genes were previously already associated with the metabolic syndrome. In conclusion, our data indicate that saturated fat (HF-PO) has a more stimulatory effect on weight gain and hepatic lipid accumulation than unsaturated fat (HF-OO and HF-SO). The overflow of fat to the distal intestine on the HF-PO diet induced changes in gut microbiota composition and mucosal gene expression. We speculate that both are directly or indirectly contributive to the saturated fat-induced development of obesity and hepatic steatosis. Keywords: Diet intervention study Nine-week-old C57Bl/6J mice were fed a low-fat diet (LF-PO) and three different types of high-fat diet, based on palm oil (HF-PO; P/S1.0), olive oil (HF-OO; P/S4.6) and safflower oil (HF-SO; P/S10.1) for 8 weeks. Body weight was recorded weekly and after 7 weeks of diet intervention an oral glucose tolerance test was performed. After 2 weeks of diet intervention, 6 mice per high-fat diet group were anaesthetized with a mixture of isofluorane (1.5%), nitrous oxide (70%) and oxygen (30%) and the small intestines were excised. Adhering fat and pancreatic tissue were carefully removed. The small intestines were divided in three equal parts along the proximal to distal axis (SI 1, SI 2 and SI 3) and microarray analysis was performed on mucosal scrapings.
2012-06-17 | E-GEOD-18586 | biostudies-arrayexpress
Project description:Periodontitis increases the risk of non-alcoholic fatty liver disease (NAFLD). However, the precise mechanisms are unclear. Here, gut dysbiosis induced by orally administered Porphyromonas gingivalis, a representative periodontopathic bacterium, was implicated in the deterioration of NAFLD pathology. C57BL/6 mice were administered with the vehicle, P. gingivalis or Prevotella intermedia, with weaker periodontal pathogenicity, followed by feeding on a choline-deficient, high fat diet (CDAHFD60). CDAHFD60 feeding induced hepatic steatosis, and combined bacterial administration further aggravated NAFLD pathology with increased fibrosis. Liver gene expression analyses revealed that genes involved in the NAFLD pathology were perturbed with distinctive expression profiles induced by different bacteria. These differences may be due to quantitative and qualitative differences in the influx of gut bacterial products because the serum endotoxin level, gut microbiota composition, and serum metabolite profile caused by ingested P. intermedia and P. gingivalis were different. These findings provide insights into mechanisms linking periodontitis and NAFLD.
2021-11-03 | GSE136937 | GEO
Project description:Mouse gut microbiota after acute high fat diet and intestinal damage
| PRJNA904807 | ENA
Project description:Purpose: Using a C57BL6/J mouse model of diet-induced obesity, we observed that mannose supplementation of high fat diet-fed mice prevents weight gain, lowers adiposity, reduces liver steatosis, and improves glucose tolerance and insulin sensitivity. Mannose increases Bacteroidetes to Firmicutes ratio of the gut microbiota, a signature previously associated with the lean phenotype. These beneficial effects of mannose are observed when supplementation is started early (3 weeks post weaning) but are lost when started later in life (8 weeks post weaning). We profiled transcriptomes of gut microbiota from high fat diet mice supplemented with or without mannose to understand the functional differences of supplementation at 3 weeks post weaning and 8 weeks post weaning. Method: Mice were weaned on high fat diet (HFD) or high fat diet with 2% mannose in drinking water (HFDM). RNA from each mouse for each diet group was isolated individually using Ambion RiboPure Bacteria kit (ThermoFisher Scientific). 1 mg cecal RNA each from 8 mice/diet group was pooled to generate 1 pool/diet for library preparation. The quality of total RNA was assessed by the Agilent Bioanalyzer Nano chip (Agilent Technologies). Total RNA was Ribo-depleted using Ribo-Zero Gold rRNA kit (Epidemiology) (Illumina). RNA-Seq library was constructed from the recovered non-ribosomal RNAs using Truseq Stranded total RNA library preparation kit (Illumina) as per the instructions. Multiplexed libraries were pooled and single-end 50-bp sequencing was performed using an Illumina Hiseq 1500. Results: The comparison of transcriptome profiles of mice supplemented with mannose at 3 weeks post weaning and 8 weeks post weaning shows mannose reduced transcript abundance for glycosyl hydrolases and carbohydrate metabolism when supplied at 3 weeks post weaning. Conclusion: The beneficial effects of mannose in responsive mice (3 weeks post weaning) are at least in part due to reduced energy harvest by gut microbes.
2018-11-06 | GSE110794 | GEO
Project description:We studied the effect of dietary fat type, varying in polyunsaturated/saturated fatty acid ratio's (P/S) on development of metabolic syndrome. C57Bl/6J mice were fed purified high-fat diets (45E% fat) containing palm oil (HF-PO; P/S 0.4), olive oil (HF-OO; P/S 1.1) or safflower oil (HF-SO; P/S 7.8) for 8 weeks. A low-fat palm oil diet (LF-PO; 10E% fat) was used as a reference. Additionally, we analyzed diet-induced changes in gut microbiota composition and mucosal gene expression. The HF-PO diet induced a higher body weight gain and liver triglyceride content compared to the HF-OO, HF-SO or LF-PO diet. In the intestine, the HF-PO diet reduced microbial diversity and increased the Firmicutes/Bacteroidetes ratio. Although this fits a typical obesity profile, our data clearly indicate that an overflow of the HF-PO diet to the distal intestine, rather than obesity itself, is the main trigger for these gut microbiota changes. A HF-PO diet-induced elevation of lipid metabolism-related genes in the distal small intestine confirmed the overflow of palm oil to the distal intestine. Some of these lipid metabolism-related genes were previously already associated with the metabolic syndrome. In conclusion, our data indicate that saturated fat (HF-PO) has a more stimulatory effect on weight gain and hepatic lipid accumulation than unsaturated fat (HF-OO and HF-SO). The overflow of fat to the distal intestine on the HF-PO diet induced changes in gut microbiota composition and mucosal gene expression. We speculate that both are directly or indirectly contributive to the saturated fat-induced development of obesity and hepatic steatosis. Keywords: Diet intervention study
2012-06-18 | GSE18586 | 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