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DNA methylation alters transcriptional rates of differentially expressed genes and contributes to pathophysiology in mice fed a high fat diet

ABSTRACT: DNA methylation alters transcriptional rates of differentially expressed genes and contributes to pathophysiology in mice fed a high fat diet

PROVIDER: PRJNA338431 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4017450_1.fastq.gz	Fastqsanger.gz
	SRR4017450_2.fastq.gz	Fastqsanger.gz
	SRR4017460_1.fastq.gz	Fastqsanger.gz
	SRR4017460_2.fastq.gz	Fastqsanger.gz
	SRR4017470.fastq.gz	Fastqsanger.gz

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DNA methylation alters transcriptional rates of differentially expressed genes and contributes to pathophysiology in mice fed a high fat diet.

Project description:ObjectiveOvernutrition can alter gene expression patterns through epigenetic mechanisms that may persist through generations. However, it is less clear if overnutrition, for example a high fat diet, modifies epigenetic control of gene expression in adults, or by what molecular mechanisms, or if such mechanisms contribute to the pathology of the metabolic syndrome. Here we test the hypothesis that a high fat diet alters hepatic DNA methylation, transcription and gene expression patterns, and explore the contribution of such changes to the pathophysiology of obesity.MethodsRNA-seq and targeted high-throughput bisulfite DNA sequencing were used to undertake a systematic analysis of the hepatic response to a high fat diet. RT-PCR, chromatin immunoprecipitation and in vivo knockdown of an identified driver gene, Phlda1, were used to validate the results.ResultsA high fat diet resulted in the hypermethylation and decreased transcription and expression of Phlda1 and several other genes. A subnetwork of genes associated with Phlda1 was identified from an existing Bayesian gene network that contained numerous hepatic regulatory genes involved in lipid and body weight homeostasis. Hepatic-specific depletion of Phlda1 in mice decreased expression of the genes in the subnetwork, and led to increased oil droplet size in standard chow-fed mice, an early indicator of steatosis, validating the contribution of this gene to the phenotype.ConclusionsWe conclude that a high fat diet alters the epigenetics and transcriptional activity of key hepatic genes controlling lipid homeostasis, contributing to the pathophysiology of obesity.

| S-EPMC5369282 | biostudies-literature

DNA methylation alters transcriptional rates of differentially expressed genes and contributes to pathophysiology in mice fed a high fat diet

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-10-01 | GSE85425 | GEO

RNA sequencing of mice fed a high fat/high sucrose diet or a low fat/low sucrose diet

Project description:Publication Title: DNA methylation alters transcriptional rates of differentially expressed genes and contributes to pathophysiology in mice fed a high fat diet. It is now well established that an intrauterine environment altered by overnutrition or malnutrition can change gene expression patterns through epigenetic mechanisms that may persist through generations. However, it is less clear if overnutrition alters epigenetic control of gene expression in adults, or if whether such mechanisms contribute to the pathology of obesity. Here we test the hypothesis that exposure to a high fat diet alters hepatic DNA methylation and gene expression patterns, and explore the contribution of such changes to the pathophysiology of overnutrition. RNA-seq and targeted high-throughput bisulfite DNA sequencing were used to undertake a systematic analysis of the hepatic response to a high fat diet. A subset of genes was found whose expression levels were altered in concert with DNA methylation changes. Using chromatin immunoprecipitation of RNA polymerase, we determined that hypermethylation correlated with decreased transcription of two of the genes, Phlda1 and Onecut1. A subnetwork of these genes and their nearest neighbors was generated from an existing Bayesian gene network that contained numerous hepatic regulatory genes involved in lipid and body weight homeostasis. Hepatic-specific depletion of Phlda1 in mice decreased the genes in the subnetwork, and led to increased oil droplet size in standard chow-fed mice, an early indicator of steatosis, validating the contribution of this gene to the phenotype.

2016-10-01 | GSE85423 | GEO

Targeted bisulfite sequencing of mice fed a high fat/high sucrose diet or a low fat/low sucrose diet

2016-10-01 | GSE85421 | GEO

TRAIL deficiency contributes to diabetic nephropathy in fat-fed ApoE-/- mice.

Project description:BackgroundWe recently demonstrated that TNF-related apoptosis-inducing ligand (TRAIL) is protective of diet-induced diabetes in mice. While TRAIL has been implicated in chronic kidney disease, its role in vivo in diabetic nephropathy is not clear. The present study investigated the role of TRAIL in the pathogenesis of diabetic nephropathy using TRAIL(-/-)ApoE(-/-) mice.MethodsTRAIL(-/-)ApoE(-/-) and ApoE(-/-) mice were fed a high fat diet for 20 w. Plasma glucose and insulin levels were assessed over 0, 5, 8 and 20 w. At 20 w, markers of kidney function including creatinine, phosphate, calcium and cystatin C were measured. Changes in mRNA expression of MMPs, TIMP-1, IL-1β and IL-18 were assessed in the kidney. Functional and histological changes in kidneys were examined. Glucose and insulin tolerance tests were performed.ResultsTRAIL(-/-)ApoE(-/-) mice had significantly increased urine protein, urine protein:creatinine ratio, plasma phosphorous, and plasma cystatin C, with accelerated nephropathy. Histologically, increased extracellular matrix, mesangial expansion and mesangial cell proliferation in the glomeruli were observed. Moreover, TRAIL(-/-)ApoE(-/-) kidneys displayed loss of the brush border and disorganisation of tubular epithelium, with increased fibrosis. TRAIL-deficient kidneys also had increased expression of MMPs, TIMP-1, PAI-1, IL-1β and IL-18, markers of renal injury and inflammation. Compared with ApoE(-/-) mice, TRAIL-/-ApoE-/- mice displayed insulin resistance and type-2 diabetic features with reduced renal insulin-receptor expression.ConclusionsHere, we show that TRAIL-deficiency in ApoE(-/-) mice exacerbates nephropathy and insulin resistance. Understanding TRAIL signalling in kidney disease and diabetes, may therefore lead to novel strategies for the treatment of diabetic nephropathy.

| S-EPMC3965481 | biostudies-literature

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Redox Imbalance in COVID-19 Pathophysiology

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Expression data from rat kidney: pathophysiology of proteinuria

Project description:This SuperSeries is composed of the following subset Series: GSE14666: Expression data from female rat kidney: pathophysiology of proteinuria GSE14676: Expression data from male rat kidney: pathophysiology of proteinuria Refer to individual Series

2009-02-03 | E-GEOD-14677 | biostudies-arrayexpress

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