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Effect of a HFrD on the EAC progression in the L2-IL1B mouse model

ABSTRACT: High-Fructose Diet accelerates early tumorigenesis in a Mouse Model of Barrett´s Esophagus through effects on the gut microbiota

PROVIDER: PRJEB48315 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR7179060_1.fastq.gz	Fastqsanger.gz
	ERR7179060_2.fastq.gz	Fastqsanger.gz
	ERR7179061_1.fastq.gz	Fastqsanger.gz
	ERR7179061_2.fastq.gz	Fastqsanger.gz
	ERR7179062_1.fastq.gz	Fastqsanger.gz

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Effect of a HFrD on the EAC progression in the L2-IL1B mouse model

Project description:High-Fructose Diet accelerates early tumorigenesis in a Mouse Model of Barrett´s Esophagus through effects on the gut microbiota

| PRJEB48315 | ENA

Project description:High-Fructose Diet accelerates early tumorigenesis in a Mouse Model of Barretts Esophagus

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High fat diet accelerates Barrett esophageal carcinogenesis by inducing a distinct IL-8 dependent immune reaction through alteration of the microbiome

Project description:Barrett Esophagus (BE) is a risk factor for the development of esophageal adenocarcinoma (EAC). As endemic obesity emerges as a risk factor for increasing numbers of EAC we utilized our IL-1b mouse model of BE to understand the impact of a high fat diet (HFD) on disease progression. Indeed, increased dysplasia development in HFD treated IL-1b mice correlated with an accelerated cytokine response with specific upregulation of IL-8 in esophageal tissue, which could be confirmed by specific overexpression of IL-8 in the BE mouse model. Consequently we observed an influx of immature myeloid cells and neutrophils resulting in a decrease of regulatory NK T cells. HFD led to a specific shift in the gut microbiome, similar to that in human BE patients, being responsible for a specific inflammatory phenotype with elevated IL-1b and IL-8 which could be eliminated under germ free conditions and lead to an increased influx of cardia (Lgr5) stem cells into the esophagus giving rise to dysplasia.

2019-04-30 | GSE103616 | GEO

Effects of fructose on liver gene expression profile in DEN-induced HCC model.

Project description:Excessive fructose consumption causes fatty liver disease and steatohepatitis, conditions that elevate liver cancer risk. Although fructose was documented to cause metabolic abnormalities and microbial dysbiosis, whether and how it triggers liver tumorigenesis was unknown. We now describe a mouse model in which fructose acts as a carcinogen, giving rise to intestinal dysbiosis and translocation of inflammation-evoking microbial products that reach the liver via the portal circulation. These inflammatory stimuli initiate hepatocellular carcinogenesis. Genetic enhancement of epithelial barrier integrity and microbiota depletion with broad spectrum antibiotics prevent fructose-induced steatosis and liver cancer.

2020-03-30 | GSE119080 | GEO

Effect ofhepatocyte-specific Chrebp knockout on model of high-fructose diet during pregnancy

Project description:During pregnancy, a high-fructose diet (HFrD) exacerbates gestational insulin resistance and is associated with an increased risk of gestational diabetes. The relationship between liver ChREBP and gestational insulin resistance remains unknown. To address this question, we fed pregnant hChrebp-KO mice and wild-type mice a high-fructose diet, and on the 17th day of pregnancy, we extracted liver tissue from the mice and conducted comparative transcriptomic analysis to elucidate the role of liver ChREBP in gestational insulin resistance."

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Exposure of squamous esophageal cell line HET-1A to deoxycholic acid (DCA)

Project description:The involvment of bile acids such as deoxycholic acid (DCA) in gastro-esophageal reflux disease and subsequent Barrett’s metaplsia has been postulated. This study examines gene expression induced by exposure to DCA in esophageal cells and may be utilised in cross-comparisions with data derived from gene expression studies of Barrett’s esophagus and associated adenocarcinoma. Additionally this study may be used to assess divergence in response to bile acids by comparisons with similar study performed in SKGT4 barrett''s assocaited adenocarcinoma cell line.

2010-02-20 | GSE13378 | GEO

Expression data from 15 month old rat brain subjected to fructose fetal programming

Project description:Fructose has recently been observed to affect brain metabolism and cognitive function in adults. However, possible fetal programming of brain metabolism induced by gestational fructose has not been examined. We evaluated mitochondrial function in the brain of aging (15 month) male offspring of Fischer F344 rat dams fed either a high-fructose diet (50% energy from fructose) or a matched control diet during early life (gestation and lactation). We used microarrays to detail changes in global programme of gene expression in offspring brains from rats subjected to either a control diet or a high fructose diet during gestation and lactation

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Exposure of squamous esophageal cell line HET-1A to deoxycholic acid (DCA)

Project description:The involvment of bile acids such as deoxycholic acid (DCA) in gastro-esophageal reflux disease and subsequent Barrettâ??s metaplsia has been postulated. This study examines gene expression induced by exposure to DCA in esophageal cells and may be utilised in cross-comparisions with data derived from gene expression studies of Barrettâ??s esophagus and associated adenocarcinoma. Additionally this study may be used to assess divergence in response to bile acids by comparisons with similar study performed in SKGT4 barrett''s assocaited adenocarcinoma cell line. HET-1A cells were exposed to 300um DCA over 24 hours in duplicate experiments including matched timepoint controls

2010-02-28 | E-GEOD-13378 | biostudies-arrayexpress

Project description:Salivary microbiome composition is associated with advanced neoplasia in Barrett esophagus

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Polyphenols protection against fructose overload

Project description:To decipher the beneficial effects of Polyphenols on health, healthy volunteers were randomized into two groups and were submitted to either a red grape polyphenol rich extract supplemented diet (PP) or a placebo diet (PCB) during 8 weeks. Then they were submitted to a fructose load (3g/kg Fat Free Mass/day) during 7 days. Muscle biopsies were taken before the protocol, 8 weeks after PP or PCB diet and after the 7 days fructose load. We have employed whole genome microarray expression profiling as a discovery platform to identify genes regulated by fructose and to identify the mechanism of action of Polyphenols. Healthy volunteers were randomized into two groups and were submitted to either a red grape polyphenol rich extract supplemented diet (PP) or a placebo diet (PCB) during 8 weeks. Then they were submitted to a fructose load (3g/kg Fat Free Mass/day) during 7 days. Muscle biopsies were taken before the protocol, 8 weeks after PP or PCB diet and after the 7 days fructose load. We have employed whole genome microarray expression profiling as a discovery platform to identify genes regulated by fructose and to identify the mechanism of action of Polyphenols. Ten biological replicates were processed for PP diet, nine for PCB diet.

2013-02-04 | E-GEOD-35764 | biostudies-arrayexpress

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