E3b06d13-1ce8-4ad3-a424-7c6e512dfcb2 - samples
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PROVIDER: EGAD00001006351 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:The link between the gut microbiota and type 2 diabetes (T2D) warrants further investigation because of known confounding effects from antidiabetic treatment. Here we profiled the gut microbiome in a discovery (n=1011) and validation (n=484) cohort comprising Swedish subjects naive for diabetes treatment and grouped by glycemic status.
| EGAS00001004480 | EGA
Project description:Metaproteomic investigation to unveil human gut microbiota features possibly linked to the onset of type 1 diabetes
2022-06-21 | MSV000089691 | MassIVE
Project description:A recently layer of gene expression regulation is N6-methyladenosine (m6A) mRNA modification. The role of gut microbiota in modulating host m6A epitranscriptomic and gene expression has not been studied. To decipher the role of gut microbiome, we profiled m6A mRNA modification epitranscriptomic mark in conventional mice compared to germ free mice. Transcriptome-wide mapping of host m6A mRNA modifications in four mice tissues allowed us to discover that gut microbiota can greatly impact host m6A mRNA modifications. The expression levels of m6A writers in mice tissues are regulated by gut microbiota. In conclusion, we report transcriptome-wide mapping of host m6A mRNA modifications regulated by gut microbiota. The present study can help better understand the role of the microbiome in host gene expression and host-microbiome interactions.
2018-12-28 | GSE120262 | GEO
Project description:The indigenous human gut microbiota is a major contributor to the human superorganism with established roles in modulating nutritional status, immunity, and systemic health including diabetes and obesity. The complexity of the gut microbiota consisting of over 1012 residents and approximately 1000 species has thus far eluded systematic analyses of the precise effects of individual microbial residents on human health. In contrast, health benefits have been shown upon ingestion of certain so-called probiotic Lactobacillus strains in food products and nutritional supplements, thereby providing a unique opportunity to study the global responses of a gut-adapted microorganism in the human gut and to identify the molecular mechanisms underlying microbial modulation of intestinal physiology, which might involve alterations in the intestinal physico-chemical environment, modifications in the gut microbiota, and/or direct interaction with mucosal epithelia and immune cells. Here we show by transcriptome analysis using DNA microarrays that the established probiotic bacterium, L. plantarum 299v, adapts its metabolic capacity in the human digestive tract for carbohydrate acquisition and expression of exo-polysaccharide and proteinaceous cell surface compounds. This report constitutes the first application of global gene expression profiling of a gut-adapted commensal microorganism in the human gut. Comparisons of the transcript profiles to those obtained for L. plantarum WCFS1 in germ-free mice revealed conserved L. plantarum responses indicative of a core transcriptome expressed in the mammalian gut and provide new molecular targets for determining microbial-host interactions affecting human health. Hybridization of the samples against a common reference of gDNA isolated from L. plantarum 299v
2010-05-16 | E-GEOD-17634 | biostudies-arrayexpress
Project description:Metformin is the therapy of choice for treating type 2 diabetes and is currently repurposed for a wide range of diseases including aging. Recent evidence implicates the gut microbiota as a site of metformin action. Combining two tractable genetic models, the bacterium E. coli and the nematode C. elegans, we performed C. elegans RNAseq to investigate the role of the metformin sensitive OP50 and metformin resistant OP50-MR E. coli microbiota in the drug effects on the host. Our data suggest an evolutionarily conserved bacterial mediation of metformin effects on host lipid metabolism and lifespan.
2019-07-13 | E-MTAB-7272 | biostudies-arrayexpress
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:Gender bias and the role of sex hormones in autoimmune diseases are well established. In specific-pathogen free (SPF) non-obese diabetic (NOD) mice females have 1.3-4.4 times higher incidence of Type 1 diabetes (T1D). Germ-free (GF) mice lose the gender bias (female/male ratio 1.1-1.2). Gut microbiota differed in males and females, a trend reversed by male castration, confirming that androgens influence gut microbiota. Colonization of GF NOD mice with defined microbiota revealed that some but not all lineages overrepresented in male mice supported a gender bias in T1D, and protection did not correlate with androgen levels. However, hormone-supported selective microbial lineage variation may work as a positive feedback mechanism contributing to the sexual dimorphism of autoimmune diseases. Gene expression analysis suggested pathways involved in protection of males from T1D by microbiota. We compared gene expression patterns in the pancreatic lymph nodes (PLNs) between four groups of mice (two genders in SPF and GF conditions, respectively). PLNs were isolated from 9-10 week old GF and SPF male and female NOD mice with 3 mice in each group, for a total of 12 samples.
2013-08-02 | E-GEOD-49467 | biostudies-arrayexpress
Project description:Gut microbiota participates in diverse metabolic and homeostatic functions related to health and well-being. Individual variation in its composition depends on many factors including dietary factors. We profiled enzymatic activity of fecal microbiota in 63 healthy adult individuals using metaproteomics, and identified Bacteroides and Prevotella –derived microbial CAZy (carbohydrate-active) enzymes involved in glycan foraging. One particular profile with many Bacteroides-derived CAZy was identified in one-third of subjects (n=20), and it associated with high abundancy of Bacteroides in most subjects. In other subjects (n=8) with dietary parameters similar to former, microbiota showed intense expression of Prevotella-derived CAZy including exo−beta−(1,4)−xylanase, xylan-1,4−beta−xylosidase, alpha−L−arabinofuranosidase and several other CAZy belonging to glycosyl hydrolase families involved in digestion of complex plant-derived polysaccharides. This associated invariably with robust representation of Prevotella in gut microbiota, while subjects with intermediate representation of Prevotella showed no CAZy profile. Identification of Bacteroides- and Prevotella-derived CAZy in microbiota proteome and their association with robust differences in microbiota composition, the latter with exceptionally high Prevotella abundancy in the gut, are in evidence of individual variation in metabolic adaptation of gut microbiota with an impact on colonizing competence.
2021-06-30 | PXD017059 | Pride
Project description:Whether myogenesis is affected by the maternal gut dysbacteriosis still remains ambiguous. In this study, firstly we show elevated level of lipopolysaccharides (LPS) in a gut microbiota dysbiosis mouse model. Secondly, we demonstrate that the diameter of muscle fibres, limb development and somitogenesis were inhibited in both gut microbiota dysbiosis and LPS exposed mice and chicken embryos. These might be due to LPS disturbed the cell survival and the key genes which regulating the somitogenesis and myogenesis. RNA sequencing and subsequent validation experiments verified that retinoic acid (RA) signaling perturbation was mainly responsible for the aberrant somite formation and differentiation. Subsequently, we found that LPS-induced Roxidative stress (ROS generation and antioxidant genes such as Nrf2, AKR) contributed to the above-mentioned interference with RA signaling. These findings highlight that the gut microbiota homeostasis also involved in regulating the development of muscle progenitor cells during pregnancy.
2020-05-08 | GSE139525 | GEO
Project description:Whether myogenesis is affected by the maternal gut dysbacteriosis still remains ambiguous. In this study, firstly we show elevated level of lipopolysaccharides (LPS) in a gut microbiota dysbiosis mouse model. Secondly, we demonstrate that the diameter of muscle fibres, limb development and somitogenesis were inhibited in both gut microbiota dysbiosis and LPS exposed mice and chicken embryos. These might be due to LPS disturbed the cell survival and the key genes which regulating the somitogenesis and myogenesis. RNA sequencing and subsequent validation experiments verified that retinoic acid (RA) signaling perturbation was mainly responsible for the aberrant somite formation and differentiation. Subsequently, we found that LPS-induced Roxidative stress (ROS generation and antioxidant genes such as Nrf2, AKR) contributed to the above-mentioned interference with RA signaling. These findings highlight that the gut microbiota homeostasis also involved in regulating the development of muscle progenitor cells during pregnancy.
2020-05-08 | GSE139422 | GEO