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E-MTAB-7884

ABSTRACT: Investigating NAFLD from RNA-seq data (human cell line Huh7) for samples under three treatments: low fat low sugar, low fat high sugar and high fat high sugar. Wild type samples are compared against DGAT2 knocked out.

PROVIDER: E-MTAB-7884 | ExpressionAtlas | 2025-01-23

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MTAB-7884-analysis-methods.tsv	Tabular
	E-MTAB-7884-analytics.tsv	Tabular
	E-MTAB-7884-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-7884-configuration.xml	Xml
	E-MTAB-7884-g1_g2-mvaPlot.png	Other

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Investigating NAFLD from RNA-seq data (human cell line Huh7) for samples under three treatments: low fat low sugar, low fat high sugar and high fat high sugar. Wild type samples are compared against DGAT2 knocked out.

Project description:Investigating NAFLD from RNA-seq data (human cell line Huh7) for samples under three treatments: low fat low sugar, low fat high sugar and high fat high sugar. Wild type samples are compared against DGAT2 knocked out.

| PRJEB32201 | ENA

Project description:Non-alcoholic fatty liver disease (NAFLD) is a major public health burden and it covers a spectrum of diseases. NAFLD starts with the accumulation of lipid droplets (LDs) within hepatocytes (steatosis). Part of the challenge of studying the mechanistic processes involved in LD accumulation and their implications on the pathogenesis of human NAFLD is due to the available models. Investigating hepatic LDs in humans is challenging and relies on liver biopsies, meaning only cross-sectional data be obtained. On the other hand, LD patterns in in vitro models are poorly defined and rarely reported. Diacylgylcerol acyltransferase (DGAT)2 is one of two enzymes that carry out the final committed step in triacylglycerol (TAG) synthesis. It is unclear whether the enzymes are able to compensate for each other or whether they have distinct roles. It has been hypothesised that DGAT1 primarily utilises exogenous fatty acids and DGAT2 uses de novo-derived fatty acids. Given the important role of this enzyme in TAG synthesis and accumulation, the aims of this study are first to create a cellular model of intrahepatocellular TAG accumulation by manipulating nutritional substrates and to investigate intracellular metabolism in wildtype and DGAT2 knockout cells under these conditions. The experimental workflow for this study is as follows: Huh7 cells (either wild type or knockout) were grown in media containing 11 mM glucose and 2% human serum (HS) for seven days before additional sugars and fatty acids (FAs) were added for a further seven days. All treatments contained 11 mM glucose and 2% HS, either with 200 µM FAs (low fat low sugar; LFLS), 5.5 mM fructose + 200 µM FAs (low fat high sugar; LFHS) or 5.5 mM fructose + 800 µM FAs (high fat high sugar; HFHS). FA metabolism, lipid droplet characteristics and transcriptomic signatures were investigated.

2020-08-21 | E-MTAB-7884 | biostudies-arrayexpress

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.

2021-11-25 | GSE140972 | GEO

E-GEOD-21601

Project description:Transcription profiling by array of Arabidopsis knocked out for bZIP1

2014-07-03 | E-GEOD-21601 | ExpressionAtlas

HuR promotes triglyceride synthesis and intestinal fat absorption

Project description:Triacylglyceride (TAG) synthesis in the small intestine determines the absorption of dietary fat, but the mechanisms underlying are largely unknown. Here, we report that the RNA-binding protein HuR (ELAVL1) promotes TAG synthesis in the small intestine. HuR associates with the 3’UTR of Dgat2 mRNA and the introns 1 of Mgat2 pre-mRNA. Association of HuR with Dgat2 3’UTR stabilizes Dgat2 mRNA, while association of HuR with intron 1 of Mgat2 pre-mRNA promotes the processing of Mgat2 pre-mRNA. Intestinal epithelium-specific HuR knockout reduces the expression of DGAT2 and MGAT2, thereby reducing the dietary fat absorption through TAG synthesis and mitigating high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) and obesity. Our findings highlight a critical role of HuR in promoting dietary fat absorption.

2024-01-10 | GSE252591 | GEO

HuR promotes triglyceride synthesis and intestinal fat absorption

2024-04-03 | GSE262777 | GEO

E-MTAB-6929

Project description:RNA-seq of mouse hypothalamus to investigate effect of high vs low fat diet

2018-11-12 | E-MTAB-6929 | ExpressionAtlas

E-GEOD-7020

Project description:Transcription profiling by array of spleens from mice with Nix knocked out.

2014-07-03 | E-GEOD-7020 | ExpressionAtlas

E-GEOD-58358

Project description:Transcription profiling by array of bone marrow from mice fed with low fat, high saturated fat or high polyunsaturated fat diets to study the potential protective effect of fat content in diet on increased septic survival and decreased bacterial load

2014-12-05 | E-GEOD-58358 | ExpressionAtlas

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.

2017-01-01 | GSE70477 | GEO

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