Ontology highlight
ABSTRACT:
PROVIDER: PRJNA993433 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Effects of different diet types on fecal microbiota in a boar model
| PRJNA993415 | ENA
Project description:We found that low protein diet consumption resulted in decrease in the percentage of normal Paneth cell population in wild type mice, indicating that low protein diet could negatively affect Paneth cell function. We performed fecal microbiota composition profiling. Male mice were used at 4-5 weeks of age. Fecal samples were collected for microbiome analysis.
2023-07-02 | E-MTAB-11277 | biostudies-arrayexpress
Project description:We found that western diet consumption resulted in decrease in the percentage of normal Paneth cell population in wild type mice, indicating that western diet could negatively affect Paneth cell function. Subsequent generations of western diet consumption further reduced percentages of normal Paneth cell population. We performed fecal microbiota composition profiling. Male mice were used at 4-5 weeks of age. Fecal samples were collected for microbiome analysis.
2023-01-01 | E-MTAB-10995 | biostudies-arrayexpress
Project description:To investigate the effects of transplanted pre-ketogenic diet (pre-KD) and post-ketogenic diet (post-KD) human fecal microbiota on recipient germ-free swiss webster brain gene expression profiles
2023-12-01 | GSE225682 | GEO
Project description:Fecal Microbiota rawdata from autistic model mice. Female and Male Poly I:C treated mice were compared at microbiota level.
2023-05-04 | E-MTAB-11150 | biostudies-arrayexpress
Project description:<p>We investigate the hypothesis that consistent changes in the human gut microbiome are associated with Crohn's disease, a form of inflammatory bowel disease, and that altered microbiota contributes to pathogenesis. Analysis of this problem is greatly complicated by the fact that multiple factors influence the composition of the gut microbiota, including diet, host genotype, and disease state. For example, data from us and others document a drastic impact of diet on the composition of the gut microbiome. No amount of sequencing will yield a useful picture of the role of the microbiota in disease if samples are confounded with uncontrolled variables.</p> <p>We aim to characterize the composition of the gut microbiome while controlling for diet, host genotype, and disease state. Diet is controlled by analyzing children treated for Crohn's disease by placing them on a standardized elemental diet, and by testing effects of different diets on the gut microbiome composition in adult volunteers. Genotype is analyzed by large scale SNP genotyping, which is already underway and separately funded--team member Hakon Hakonarson is currently genotyping 50 children a week at ~half a million loci each and investigating connections with inflammatory bowel disease. Clinical status is ascertained in the very large IBD practice in the UPenn/CHOP hospital system. Effects of diet, host genotype, and disease state on the gut microbiome are summarized in a multivariate model, allowing connections between microbiome and disease to be assessed free of confounding factors.</p> <p>This project is divided into four sub-studies. In the Fecal Storage Methods (FSM) study, methods of stool storage and DNA extraction are compared to examine their impact on DNA sequence analysis results. The Controlled Feeding Experiment (CaFE) addresses the effects of controlled diets on the gut microbiome. In the Cross-sectional Study of Diet and Stool Microbiome Composition (COMBO), the effects of diet analyzed using surveys and deep sequencing of stool specimens. The fourth study, Pediatric Longitudinal Study of Elemental Diet and Stool Microbiome Composition (PLEASE), examines the effects of an elemental diet treatment on pediatric patients diagnosed with inflammatory bowel disease (IBD), particularly Crohn's disease.</p> <p> <ul> <li>Fecal Storage Methods (FSM): Cross-sectional study</li> <li>Controlled Feeding Experiment (CaFE): Controlled trial</li> <li>Cross-sectional Study of Diet and Stool Microbiome Composition (COMBO): Cross-sectional study</li> <li>Pediatric Longitudinal Study of Elemental Diet and Stool Microbiome Composition (PLEASE): Longitudinal cohort study</li> </ul> </p>
| phs000252 | dbGaP
Project description:Aconitate decarboxylase 1 (ACOD1) is the enzyme synthesizing itaconate, an immuno-regulatory metabolite tuning host-pathogen interactions. Such functions are achieved by affecting metabolic pathways regulating inflammation and microbe survival. However, at the whole-body level, metabolic roles of itaconate remain largely unresolved. By using multiomics-integrated approaches, here we show that ACOD1 responds to high-fat diet consumption in mice by promoting gut microbiota alterations supporting metabolic disease. Genetic disruption of itaconate biosynthesis protects mice against obesity, alterations in glucose homeostasis and liver metabolic dysfunctions by decreasing meta-inflammatory responses to dietary lipid overload. Mechanistically, fecal metagenomics and microbiota transplantation experiments demonstrate such effects are dependent on an amelioration of the intestinal ecosystem composition, skewed by high-fat diet feeding towards obesogenic phenotype. In particular, unbiased fecal microbiota profiling and axenic culture experiments point towards a primary role for itaconate in inhibiting growth of Bacteroidaceae and Bacteroides, family and genus of Bacteroidetes phylum, the major gut microbial taxon associated with metabolic health. Specularly to the effects imposed by Acod1 deficiency on fecal microbiota, oral itaconate consumption enhances diet-induced gut dysbiosis and associated obesogenic responses in mice. Unveiling an unrecognized role of itaconate, either endogenously produced or exogenously administered, in supporting microbiota alterations underlying diet-induced obesity in mice, our study points ACOD1 as a target against inflammatory consequences of overnutrition.
2024-02-05 | GSE213632 | GEO
Project description:Microbial RNAseq analysis of cecal and fecal samples collected from mice colonized with the microbiota of human twins discordant for obesity. Samples were colleted at the time of sacrifice, or 15 days after colonization from mice gavaged with uncultured or cultured fecal microbiota from the lean twins or their obese co-twins. Samples were sequenced using Illumina HiSeq technology, with 101 paired end chemistry. Comparisson of microbial gene expression between the microbiota of lean and obese twins fed a Low fat, rich in plant polysaccharide diet.
2013-10-01 | E-GEOD-48861 | biostudies-arrayexpress
Project description:Habitual exercise modulates the composition of the intestinal microbiota. We examined whether transplanting fecal microbiota from trained mice improved skeletal muscle metabolism in high-fat diet-fed mice. The recipient mice that received fecal samples from trained donor mice for 1 week showed elevated levels of metabolic signalings in skeletal muscle. Glucose tolerance was improved by fecal microbiota transplantation after 8 weeks of HFD administration. Intestinal microbiota may mediate exercise-induced metabolic improvement in mice. We performed a microarray analysis to compare the metabolic gene expression profiles in the skeletal muscle from each mouse.
2022-06-30 | GSE201202 | GEO
Project description:Compositional changes in the microbiota (dysbiosis) may be a basis for Irritable Bowel Syndrome (IBS) but biomarkers are currently unavailable to direct microbiota-directed therapy. We therefore examined whether changes in fecal β-defensin could be a marker of dysbiosis in a murine model. Experimental dysbiosis was induced using four interventions relevant to IBS: a mix of antimicrobials, westernized diets (high-fat/high-sugar and, high salt diets), or mild restraint stress. Fecal mouse β-defensin-3 and 16S rRNA-based microbiome profiles were assessed at baseline, during and following these interventions. Each intervention, except for mild restraint stress, altered compositional and diversity profiles of the microbiota. Exposure to antimicrobials or a high-fat/high-sugar diet, but not mild restraint stress, resulted in decreased fecal β-defensin-3 compared to baseline. In contrast, exposure to the high salt diet increased β-defensin-3 compared to baseline but this was not accompanied by discernible inflammatory changes in the host.
2023-07-11 | GSE225272 | GEO