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Hepatocyte RNA-seq analysis in liver-specific XBP1 knockout mice fed a high fat sugar diet

ABSTRACT: Hepatocyte RNA-seq analysis in liver-specific XBP1 knockout mice fed a high fat sugar diet

PROVIDER: PRJNA789155 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17260757.fastq.gz	Fastqsanger.gz
	SRR17260759.fastq.gz	Fastqsanger.gz
	SRR17260763.fastq.gz	Fastqsanger.gz
	SRR17260764.fastq.gz	Fastqsanger.gz

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Hepatocyte RNA-seq analysis in liver-specific XBP1 knockout mice fed a high fat sugar diet

Project description:X-box binding protein 1 (XBP1) is a key component of the unfolded protein response (UPR) and plays important roles in the pathogenesis of nonalcoholic fatty liver diseases (NAFLD). Mice with liver-specific XBP1 deletion developed great liver injury and fibrosis in a dietary model of NAFLD. This project is to investigate hepatocyte-specific transcriptome profiling in XBP1-deficient mice fed a high fat sugar diet.

2022-01-03 | GSE190947 | GEO

Hepatic transcriptome profiling of liver-specific Xbp1 knockout mice fed a high fat diet

Project description:Xbp1 is an important regulator of unfolded protein response and lipid metabolism. Its dyregulation has been associcated in human NASH. Feeding a high fat diet with fructose/sucrose to mice causes progressive, fibrosing steatohepatitis. This study is to use RNA-Seq to identify differentially expressed genes in hepatic Xbp1 deficient mice livers fed with a high fat diet compared to controls. Hepatic Xbp1 deficient mice or flox controls were fed either regular chow or a high fat diet (n=4). Samples from each cohort were pooled into two replicates.

2016-01-07 | E-GEOD-64824 | biostudies-arrayexpress

Hepatic transcriptome profiling of liver-specific Xbp1 knockout mice fed a high fat diet

2016-01-07 | GSE64824 | GEO

RNA-next generation sequencing of intestine tissue from mice fed high fat diet or/and sugar drink

Project description:Purpose: NGS was used to determine if a distinct transcriptomic profile is observed among the experimental mice fed four different dietary components. Methods: We carried out RNA-Seq analysis of ileum tissue from 6 weeks male mice ad libitum fed for 10 weeks a high liquid sugar (23% (w/v)) or/and high fat (60% Kcal from fat) diet. The combined effect of sugar drink and high fat diet (HF-Sugar) was compared with sugar drink only (NF-Sugar), or high fat diet only (HF), or control diet that was plain water and normal fat diet (NF). Results: RNA-Seq revealed sample-specific clusters that included genes responding to each experimental diet. We found only addition of sugar drink to high fat group (HF-Sugar) not NF-Sugar and HF, there was a significant enrichment in biological functions relating to Inflammatory/Immune Responses, especially including dendritic cell (DC) and T cell related signaling pathway. Conclusions: Taken together, our data demonstrate that sugar drink synergistically promotes and exacerbates inflammatory responses driven by the high fat diet.

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HIgh fat refined sugar diet and hippocampus

Project description:Rats were fed either a control diet or high fat and refined sugar (HFS) diet and hippocampus was resected for proteomic analysis

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Differential transcriptional networks regulated by high sugar consumption in normal and high-fat-fed mice

Project description:High sugar consumption, as well as high-fat diet, is a known cause of obesity and metabolic syndrome. However, the synergistic effect of high-sugar and high-fat consumption rarely has been evaluated, especially in terms of transcriptional regulation. Therefore, we focused on the effect of high sugar consumption on hepatic transcriptional networks in normal and high fat-fed mice. C57BL/6J mice were divided into four groups and were provided either 23%(w/v) sugar solution or plain water with either high-fat or normal-fat diet for 10 weeks. As a result, high sugar consumption significantly altered lipid metabolism-related genes in normal fat-fed mice; however, in high fat-fed mice, high sugar consumption altered inflammation-responsive genes rather than lipid metabolism. After all, these modulations eventually increased lipid accumulation in the liver and caused systemic metabolic disturbances. These observations for the first time suggested that high sugar consumption along with high-fat diet could lead to the development of severe metabolic syndrome via altering hepatic transcriptional networks.

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RNA-seq expression analysis of liver, adipose, skeletal muscle, heart, and pancreatic islets from DO founder strain mice fed high-fat, high-sugar diet. [Islet]

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RNA-seq expression analysis of liver, adipose, skeletal muscle, heart, and pancreatic islets from DO founder strain mice fed high-fat, high-sugar diet. [Adipose]

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