Ontology highlight
ABSTRACT:
PROVIDER: PRJNA939937 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23697661_1.fastq.gz | Fastqsanger.gz | |||
| SRR23697661_2.fastq.gz | Fastqsanger.gz | |||
| SRR23697662_1.fastq.gz | Fastqsanger.gz | |||
| SRR23697662_2.fastq.gz | Fastqsanger.gz | |||
| SRR23697663_1.fastq.gz | Fastqsanger.gz |
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Project description:Obstruction of bile flow results in bacterial proliferation and mucosal injury in the small intestine that can lead to the translocation of bacteria across the epithelial barrier and systemic infection. These adverse effects of biliary obstruction can be inhibited by administration of bile acids. Here we show that the farnesoid X receptor (FXR), a nuclear receptor for bile acids, induces genes involved in enteroprotection and inhibits bacterial overgrowth and mucosal injury in ileum caused by bile duct ligation. Mice lacking FXR have increased ileal levels of bacteria and a compromised epithelial barrier. These findings reveal a central role for FXR in protecting the distal small intestine from bacterial invasion and suggest that FXR agonists may prevent epithelial deterioration and bacterial translocation in patients with impaired bile flow. In this report we have examined the role of FXR in the ileum. We demonstrate that it plays a crucial role in preventing bacterial overgrowth and maintaining the integrity of the intestinal epithelium
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Project description:To investigate the role of bile acids in regulating intestinal epithelium differentiation, mouse small intestinal organoids cultured for 2 days were incubated with a series of bile acids at 50 mmol/L for 96 hours and lysed for RNA extraction.
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Project description:Primary bile acids are produced in the liver whereas secondary bile acids such as lithocholic acid (LCA) are generated by gut bacteria from primary bile acids that escape the ileal absorption. Besides their well-known function as detergents in lipid digestion, bile acids are important signaling molecules mediating effects on the host’s metabolism. As energy metabolism is closely linked to aging and longevity we supplemented fruit flies (Drosophila melanogaster) with 50 µmol/l LCA either for 30 days or throughout their lifetime. LCA supplementation resulted in a significant induction of the mean (+12 days), median (+10 days) and maximum lifespan (+ 11 days) in comparison to untreated control flies. This lifespan extension was accompanied by an induction of spargel (srl), the fly homolog of mammalian PPARG co-activator 1a(PGC1A. In srl mutant flies, LCA failed to induce longevity emphasizing the essential role of srl in the observed lifespan extension. In addition, the administration of antibiotics to wild type flies abrogated LCA-mediated effects on both lifespan and srl expression, suggesting a substantial contribution of the intestinal microbiota to the LCA-induced longevity. In the present study, we show that the secondary bile acid LCA significantly induced the mean, the median and the maximum survival in Drosophila melanogaster. Our data suggest that besides an up-regulation of the PGC1a-homolog srl unidentified alterations in the structure or metabolism of gut microbiota contribute to the longevity effect of LCA.
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Project description:In addition to their role as a digestive detergent, bile acids have the ability to modulate the expression of genes. The intestinal content of cholic acids (CA) fluctuated in response to the daily feeding-fasting cycle; therefore, we hypothesized that the temporal accumulation of CA may affect the expression of genes in intestinal epithelial cells. To screen bile acid-regulated genes, we performed oligonucleotide microarray analyses using RNA isolated from the CA-treated intestinal cells of mice. Several types of genes were screened as candidates for bile acid-regulated genes. They included genes that encoded lipid metabolism-related proteins, receptors, transcriptional factors, and plasma-membrane transporters. Total 2 samples were derived from [1] vehicle (0.05% DMSO and 0.25% ethanol)-treated intestinal epithelial cells of mice and [2] cholic acid (CA)-treated intestinal epithelial cells of mice.
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Project description:In addition to their role as a digestive detergent, bile acids have the ability to modulate the expression of genes. The intestinal content of cholic acids (CA) fluctuated in response to the daily feeding-fasting cycle; therefore, we hypothesized that the temporal accumulation of CA may affect the expression of genes in intestinal epithelial cells. To screen bile acid-regulated genes, we performed oligonucleotide microarray analyses using RNA isolated from the CA-treated intestinal cells of mice. Several types of genes were screened as candidates for bile acid-regulated genes. They included genes that encoded lipid metabolism-related proteins, receptors, transcriptional factors, and plasma-membrane transporters.
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Project description:There is increased interest in the potential protective role of dietary Ca in the development of metabolic disorders related to the metabolic syndrome. Ca-induced intestinal precipitation of fatty acids and bile acids as well as systemic metabolic effects of Ca on adipose tissue is proposed to play a causal role. In this experiment, we have studied all these aspects to validate the suggested protective effect of Ca supplementation, independent of other dietary changes, on the development of diet-induced obesity and insulin resistance. In our diet intervention study, C57BL/6J mice were fed high-fat diets differing in Ca concentrations (50 v. 150 mmol/kg). Faecal excretion analyses showed an elevated precipitation of intestinal fatty acids (2·3-fold; P < 0·01) and bile acids (2-fold; P < 0·01) on the high-Ca diet. However, this only led to a slight reduction in fat absorption (from 98 to 95 %; P < 0·01), mainly in the distal small intestine as indicated by gene expression changes. We found no effect on body-weight gain. Lipolysis and lipogenesis-related parameters in adipose tissue also showed no significant changes on the high-Ca diet, indicating no systemic effects of dietary Ca on adiposity. Furthermore, early gene expression changes of intestinal signaling molecules predicted no protective effect of dietary Ca on the development of insulin resistance, which was confirmed by equal values for insulin sensitivity on both diets. Taken together, our data do not support the proposed protective effect of dietary Ca on the development of obesity and/or insulin resistance, despite a significant increase in fecal excretion of fatty acids and bile acids. Keywords: Diet intervention study Nine-week-old mice were fed a high fat purified diet with a low calcium concentration of 50mmol/kg (LCa diet) or a high calcium concentration of 150mmol/kg (HCa diet) for 8 weeks. Body weight was recorded weekly and after 7 weeks of diet intervention an oral glucose tolerance test was performed. For microarray analysis, after 2 weeks of diet intervention, 6 mice per 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 pooled mucosal scrapings.
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