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

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

PROVIDER: PRJNA591593 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10529500.fastq.gz	Fastqsanger.gz
	SRR10529501.fastq.gz	Fastqsanger.gz
	SRR10529502.fastq.gz	Fastqsanger.gz
	SRR10529503.fastq.gz	Fastqsanger.gz
	SRR10529504.fastq.gz	Fastqsanger.gz

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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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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. [heart]

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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]

2024-05-13 | GSE266921 | GEO

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

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