Ontology highlight
ABSTRACT:
PROVIDER: PRJNA971990 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24525967.fastq.gz | Fastqsanger.gz | |||
| SRR24525968.fastq.gz | Fastqsanger.gz | |||
| SRR24525969.fastq.gz | Fastqsanger.gz | |||
| SRR24525970.fastq.gz | Fastqsanger.gz | |||
| SRR24525971.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 14 |
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Project description:To understand how changes in dietary fiber consumption and SFB colonization impact small intestinal epithelial cells (IECs) and consequently intraepithelial lymphocytes.
2025-01-22 | GSE277294 | GEO
Project description:The small intestine is responsible for nutrient absorption and it is one of the most important interfaces between the environment and our body. During aging, changes in the structure of the epithelium lead to food malabsorption and reduced barrier function thus increasing disease risk in aging. The molecular drivers of these alterations remain poorly understood. Here, we compared the proteomes of small intestinal crypts from mice across different anatomical regions and age groups. We found that aging alters epithelial immune responses, metabolic networks and stem cell proliferation, and it is accompanied by a region-dependent skewing in the cellular composition of the intestinal epithelium. Of note, a short period of dietary restriction followed by re-feeding partially restores the epithelium to a youthful state by promoting the differentiation of intestinal stem cells (ISCs) towards the secretory lineage. Using in vitro and in vivo studies, we identify Hmgcs2 (3-hydroxy-3-methylglutaryl-CoA synthetase 2) – the rate limiting enzyme in the synthesis of ketone bodies – as a modulator of ISCs differentiation, which responds to dietary changes. This study provides an atlas of age-dependent proteome changes in defined regions of the intestinal epithelium and characterizes how young and old mice adapt to drastic changes of diet, such as dietary restriction and re-feeding.
2020-04-29 | PXD014311 | Pride
Project description:Eating habits are closely related to the body's nutrient absorption and metabolic homeostasis. In order to better reveal the changes of intestinal epithelial cells under different dietary patterns, we examined the changes of gene expression profiles in jejunal epithelial cells of mice after 10 days of breakfast skipping feeding pattern by RNA sequencing.
2025-01-22 | GSE256482 | GEO
Project description:Background: Human intestinal tissue samples are barely accessible to study potential health benefits of nutritional compounds. Dietary fibres have been descirbed to be beneficial for intestinal health. Therefore, in this study we explored the applicability of an in vitro model, namely human intestinal Caco-2 cells, to study the effect of dietary fibres on intestinal health. Transcriptomics was applied to obtain more insight into their mode of actions in the intestinal cells. Methods: Caco-2 cells were stimulated with 500 ug/ml dietary fibres and the maximal observed LPS contamination to serve as background control for 6 hours, total RNA was extracted and Affymterix Human Gene 1.1 ST arrays were used to analyze the gene expression profiles. To identify dietary fibre induced gene expression profiles in dietary fibre gene responses were compared to medium samples. Furthermore, to analyse differentiatlly affected pathways Ingenuite Pathway Analysis was employed. Results: Pathway analysis revealed a distinct separation between the dietary fibres. GOS and beta-glucan oat medium viscosity affected transcription of a lower amount of genes (gene cut-off p<0.05) and gen transcription changes suggest an increase in vesicle transport and altered cholesterol regulation. On the other hand, the other dietary fibres differentially regulated a larger numbers of genes (gene cut-off p<0.05) and all appeared related to immune responses. We observed an increase in intracellular and extracellular anti-bacterial pathways and production of cytokines specifically aimed at communication with the adaptive immune system. Conclusion: GOS and beta-glucan oat medium viscosity appeared to induce intestinal epithelial communication with the body, whereas the other dietary fibres appeared recognized as PAMP and induce epithelial cells to interact with the immune system.
2022-05-30 | GSE99610 | GEO
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.
2025-08-22 | PXD059757 | Pride
Project description:Obesity and related metabolic disorders are often characterized by chronic adipose tissue inflammation, driving systemic insulin resistance and general metabolic dysfunction. Free Fatty Acid Receptor 2 (FFA2) has emerged as a potential modulator of adipocyte function, inflammation, and metabolism. To investigate the role of FFA2 expressed in the adipose tissue, we generated adipose-specific FFA2 knockout mice (Adipoq-F2-KO) and assessed metabolic outcomes under standard chow and high-fat, high-sugar Western diet conditions, with and without dietary fiber supplementation. We found that adipose-specific FFA2 deletion had minimal metabolic consequences under standard dietary conditions but significantly reduced body weight and adiposity when mice were fed a fiber (fructooligosaccharide)-supplemented Western diet. Subsequent fecal analyses and transcriptomic profiling indicated impaired intestinal lipid absorption as the primary driver of reduced adiposity, suggesting disrupted adipose-intestinal communication. Unexpectedly, the lighter Adipoq-F2-KO mice also exhibited heightened adipose inflammation, characterized by increased macrophage infiltration and pro-inflammatory cytokine expression. Furthermore, in vitro loss-of-function experiments in adipocytes revealed that FFA2 knockdown impaired adipocyte maturation, lipid storage, and anti-inflammatory signaling. Additional studies using intestinal epithelial cells exposed to adipocyte-conditioned media implicated adipose-derived signals in driving intestinal dysfunction. Collectively, our findings highlight adipose-specific FFA2 as critical in regulating adipose tissue inflammation, lipid metabolism, and inter-organ communication. The data uploaded here specifically contains the comparison of mRNA from mature white adipocytes of FFA2 fl/fl mice compared to RNA from Adipoq-F2-KO mice when both are on a normal chow diet.
2025-09-30 | GSE309021 | GEO
Project description:Obesity and related metabolic disorders are often characterized by chronic adipose tissue inflammation, driving systemic insulin resistance and general metabolic dysfunction. Free Fatty Acid Receptor 2 (FFA2) has emerged as a potential modulator of adipocyte function, inflammation, and metabolism. To investigate the role of FFA2 expressed in the adipose tissue, we generated adipose-specific FFA2 knockout mice (Adipoq-F2-KO) and assessed metabolic outcomes under standard chow and high-fat, high-sugar Western diet conditions, with and without dietary fiber supplementation. We found that adipose-specific FFA2 deletion had minimal metabolic consequences under standard dietary conditions but significantly reduced body weight and adiposity when mice were fed a fiber (fructooligosaccharide)-supplemented Western diet. Subsequent fecal analyses and transcriptomic profiling indicated impaired intestinal lipid absorption as the primary driver of reduced adiposity, suggesting disrupted adipose-intestinal communication. Unexpectedly, the lighter Adipoq-F2-KO mice also exhibited heightened adipose inflammation, characterized by increased macrophage infiltration and pro-inflammatory cytokine expression. Furthermore, in vitro loss-of-function experiments in adipocytes revealed that FFA2 knockdown impaired adipocyte maturation, lipid storage, and anti-inflammatory signaling. Additional studies using intestinal epithelial cells exposed to adipocyte-conditioned media implicated adipose-derived signals in driving intestinal dysfunction. Collectively, our findings highlight adipose-specific FFA2 as critical in regulating adipose tissue inflammation, lipid metabolism, and inter-organ communication. The data uploaded here specifically contains the comparison of mRNA from mature white adipocytes of FFA2 fl/fl mice compared to RNA from Adipoq-F2-KO mice when both are on a normal chow diet.
2025-09-23 | GSE302985 | GEO
Project description:We have performed quantitative proteomic TandemMassTag to investigate proteomic changes after deletion of epigenetic eraser genes Hdac1 and Hdac2 in intestinal epithelial cells. Both HDAC1 and HDAC2 are epigenetic erasers that drive specific and redundant gene expression patterns, in part by removing acetyl groups on histones. Deletion of these Hdac in intestinal epithelial cell (IEC) in vivo alters intestinal homeostasis, dependent on the Hdac deleted and the level of expression of both. To determine the specific IEC function of HDAC1 and HDAC2, we have performed transcriptomic and quantitative proteomic approaches on IEC deficient in Hdac1 and Hdac2. We have defined changes in both mRNA and protein expression patterns affecting IEC differentiation. We have identified IEC Hdac1- and Hdac2-dependent common as well as specific pathways and biological processes. These findings uncover unrecognized similarities and differences between Hdac1 and Hdac2 in IEC.
2021-09-09 | PXD022558 | Pride
Project description:Acute, reversible dietary effect on the transcriptomic profiles of intestinal epithelial cells
| PRJNA779447 | ENA