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ABSTRACT: The influence of edible mushroom polysaccharides on the transcriptomics of mice fed a high-fat diet

PROVIDER: PRJNA1276878 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR34006257.fastq.gz	Fastqsanger.gz
	SRR34006258.fastq.gz	Fastqsanger.gz
	SRR34006259.fastq.gz	Fastqsanger.gz
	SRR34006260.fastq.gz	Fastqsanger.gz
	SRR34006261.fastq.gz	Fastqsanger.gz

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Project description:Effect of edible mushroom polysaccharides on the intestinal flora of mice fed a high-fat diet

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Effect of hepatocyte-specific PPARgamma (PPARg)expression and diet-induced NASH in the liver transcriptome of male and female mice with pre-stablished diet-induced obesity

Project description:Adult PPARg floxed male and female mice were fed a high fat diet (HFD) for 16 weeks to induce obesity. Half of these mice were then injected with AAV8-TBG-Cre to knockout PPARg in hepatocytes. The remaining half were injected with AAV8-TBG-Null to generate control mice. After two weeks, mice fed the HFD were either maintained on this diet or switched to a high fat, high cholestrol, high fructose (HFCF) diet for an additional 16 weeks. This study was designed to examine whether the loss of hepatocyte PPARg in mice with established obesity would alter the liver transcriptomics in a PPARg dependent manner when the mice are fed a HFD or a HFCF diet.

2023-01-11 | GSE200352 | GEO

Systems analysis of hepatic insulin resistance identifies RGS4 as a key mediator of metabolic adaptation

Project description:We profiled the transcriptomes of chow diet-fed and high-fat diet-fed mice across insulin stimulation time points. We also profiled the effects of metformin treatment on mouse liver transcritomes. Our temporal analyses of chow-diet and 16 week high-fat diet transcriptomics following insulin stimulation uncovered several regulator of G-protein signaling genes, particularly Rgs4, that are specifically regulated transcriptionally in HFD livers following insulin stimulation. We validated these findings with additional assays of RGS4 mRNA and protein levels and characterized this molecule's role in regulating hepatic insulin responses in mice.

2019-01-31 | GSE92488 | GEO

transcription profiling by array of C57BL/6J mice fed a Western-style diet with or without 0.05% quercetin against mice on a control diet to study the effect of quercetin on obesity and hepatic gene expression

Project description:To determine the effect of consumption of a quercetin-rich diet on obesity and dysregulated hepatic gene expression, C56BL/6J mice were fed for 20 weeks on control or a Western diet high in fat, cholesterol and sucrose, both with or without 0.05% quercetin. Chronic dietary intake of quercetin reduced body weight gain and visceral and liver fat accumulation, and improved hyperglyceamia, hyperinsulinaemia, dyslipidaemia in mice fed a Western-style diet. Feeding a Western-style diet altered expression of genes related to inflammatory responses, lipid metabolism and oxidative phosphorylation in C57BL/6J mice after 20 weeks. The results from exhaustive gene expression analysis showed that quercetin minimally influenced hepatic gene expression in mice fed the Western diet. The gene screening results (GSEA) were consistent with the notion that it did improve mitochondrial function to some extent. Quantitative RT-PCR analysis indicated that quercetin did influence important regulators of fat accumulation and metabolic disorders. Our results suggest that quercetin reduces fat accumulation presumably through decreasing oxidative stress and increasing PPARα expression, and the following improvement of gene expression related to steatosis in the liver. C56BL/6J mice were fed for 20 weeks on AIN93G (con) or a Western diet high in fat, cholesterol and sucrose, both with or without 0.05% quercetin for 20 weeks.

2012-05-29 | E-GEOD-38141 | biostudies-arrayexpress

An ‘omics approach to unraveling the paradoxical effect of diet on perfluorooctanesulfonic acid (PFOS) and perfluorononanoic acid (PFNA) induced non-alcoholic fatty liver disease (NAFLD)

Project description:Perfluoroalkyl substances (PFASs) are a family of toxicants universally detected in human serum and known to cause dyslipidemia in animals and humans. Non-alcoholic fatty liver disease (NAFLD) is most prevalent form of liver disease in the United States and has been rising in global prevalence over recent years. This study explored diet-PFAS interactions and their potential role in the increasing global incidence of NAFLD. Male C57BL/6 mice were fed with either a low-fat diet (10% kcal from fat) or a moderately high fat diet (45% kcal from fat) with or without perfluorooctanesulfonic acid (PFOS) or perfluorononanoic acid (PFNA) at a low dose of 0.0003% w/w in feed for 12 weeks. Livers were excised for histology and quantification of PFASs and lipids. Proteomics and transcriptomics were utilized to conduct mechanistic pathway exploration. In a high fat diet, PFOS and PFNA protected against the onset of hepatic lipid accumulation and inflammatory progression. Genes and proteins related to lipid metabolism, synthesis, transport, and storage were modulated by PFAS exposure and further impacted by the presence of dietary fat. When combined with a high fat diet, low dose PFOS and PFNA are protective against the onset of NAFLD suggesting that dietary fat impacts the behavior of PFASs in vivo. Furthermore, both dietary fat content and the chemical functional head group exerted significant influence on tissue partitioning and the resulting hepatic biochemical signature.

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RNAseq data of frontal cortex of 4 months high fat diet fed WT, AKO, 4 months high fat diet fed conditional human amylin expressing mice followed by vehicle and Tamoxifen injection, and 2 months high fat diet fed WT mice

Project description:We performed gene expression profiling analysis using data from RNAseq of brain frontal cortex from four months high fat diet fed WT (n=10), AKO (n=10), four months high fat diet fed condition human amylin mice followed by vehicle (n=10) or Tamoxifen (n=10) injection for another two months, and 2 months high fat diet fed WT mice (n=10).

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Protein affects gene expression and prevents lipid accumulation in the liver in mice

Project description:Obesity and associated increased prevalence of non-alcoholic fatty liver (NAFLD) disease is suggested to be positively modulated by a high protein (HP) diet in humans and rodents. The aim was to detect mechanisms by which a HP diet prevents hepatic lipid accumulation by means of transcriptomics. To study the acute and long term effect of a high protein ingestion on hepatic lipid accumulation under both low and high fat (HF) conditions, mice were fed combinations of high (35%) or low (10%) fat and high (50%) or normal (15%) protein diets for 1 or 12 weeks. Body composition, liver fat, VLDL production rate and gene expression were investigated. Differences in metabolic processes and functions in the liver were identified using gene set enrichment analysis on microarray data. Mice fed the HP diets developed less adiposity and decreased hepatic lipid accumulation due a combination of induced processes mainly involved in protein catabolism such as transamination, TCA cycle and oxidative phosphorylation. Feeding a HP diet can successfully prevent the development of NAFLD by using ingested energy for oxidation instead of storage. Wild type mice were fed combinations of high (35%) or low (10%) fat and high (50%) or normal (15%) protein diets for 1 or 12 weeks. After the diet intervention period, the animals were killed and liver tissue was removed. Total RNA was isolated, pooled and subjected to gene expression profiling.

2012-11-21 | E-GEOD-37897 | biostudies-arrayexpress

Lungs from CYP1B1 knockout mice (or controls) fed a western diet for 10 weeks

Project description:Adult CYP1B1 knockout mice (constitutive) fed a high fat diet for 10 weeks, compared to WT mice on a high fat diet

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Liver proteomic assessment of mice fed high carbohydrate and high fat diets identify a disconnect between proteins associated with de novo lipogenesis and fat

Project description:De novo lipogenesis (DNL) has been implicated in the development and progression of hepatic liver steatosis. Hepatic DNL is strongly influenced by dietary macronutrient composition with diets high in carbohydrate increasing DNL and diets high in fat decreasing DNL. The enzymes in the core DNL pathway have been well characterised however less is known about proteins that play accessory or regulatory roles in DNL. In the current study, we associate measured rates of hepatic DNL and liver fat content with abundance of liver proteins from liquid chromatography mass spectrometry in mice to identify known and uncharacterised proteins that may have a role in DNL. Male C57BL/6J mice were fed either a standard chow diet a semi-purified high starch diet or a high fat diet. Both semi-purified diets resulted in increased body weight, fat mass and liver triglyceride content compared to chow-fed mice while hepatic DNL was increased in the high starch fed mice and decreased in the high fat fed mice. Proteomic analysis was carried out on the livers of these mice and proteins were identified that associated with either the rate of DNL or triglyceride content in the liver. There was no overlap between DNL and triglyceride associated proteins. We identify novel proteins associated with DNL that are involved in taurine metabolism, which suggests a link between these pathways. Further analysis identified proteins that are differentially regulated when comparing a non-purified chow diet to either of the semi-purified diets to provide a set of proteins that are regulated by the degree of dietary complexity alone. Finally, we compared the liver proteome between 4 week-fed and 30-week diet-fed mice and found remarkable similarity suggesting that the majority of diet-regulated proteins change early in response to differing dietary components.

2024-10-30 | PXD054323 | Pride

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