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Ppara and fatty acid oxidation coordinate hepatic transcriptional architecture (ChIP-Seq)

ABSTRACT: Ppara and fatty acid oxidation coordinate hepatic transcriptional architecture (ChIP-Seq)

PROVIDER: PRJNA742025 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14931017.fastq.gz	Fastqsanger.gz
	SRR14931018.fastq.gz	Fastqsanger.gz
	SRR14931019.fastq.gz	Fastqsanger.gz
	SRR14931020.fastq.gz	Fastqsanger.gz
	SRR14931021.fastq.gz	Fastqsanger.gz

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Ppara and fatty acid oxidation coordinate hepatic transcriptional architecture

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Ppara and fatty acid oxidation coordinate hepatic transcriptional architecture (ATAC-Seq)

Project description:Mice harboring a liver-specific carnitine palmityltransferase 2 (Cpt2) knockout exhibit drastic lipid accumulation following a 24hr fast. Crossing Cpt2L-/- mice with Pparα-/- mice provides a model to drive ligand-activated Pparα signaling in liver. We use this to investigate unique patterns of Pparα target gene transcription and demonstrate the requirement for ligand-activated Pparα in maintaining transcriptionally permissive genomic architecture in liver, including regulation of promoters and enhancer elements during periods of nutrient deprivation.

2021-06-29 | GSE179050 | GEO

Ppara and fatty acid oxidation coordinate hepatic transcriptional architecture (ChIP-Seq)

Project description:Mice harboring a liver-specific carnitine palmityltransferase 2 (Cpt2) knockout exhibit drastic lipid accumulation following a 24hr fast. Crossing Cpt2L-/- mice with Pparα-/- mice provides a model to drive ligand-activated Pparα signaling in liver. We use this to investigate unique patterns of Pparα target gene transcription and demonstrate the requirement for ligand-activated Pparα in maintaining transcriptionally permissive genomic architecture in liver including regulation of promoters and enhancer elements during periods of acute nutrient deprivation.

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Ppara and fatty acid oxidation coordinate hepatic transcriptional architecture

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Carnitine Palmitoyltransferase 1 facilitates fatty acid oxidation in a noncell autonomous manner [TKO_RNAseq]

Project description:Mitochondrial fatty acid oxidation is facilitated by the combined activities of Carnitine Palmitoyltransferase 1 and Carnitine Palmitoyltransferase 2 which generate and utilize acylcarnitines respectively. We compared the response of mice with liver specific deficiencies in Cpt1a and Cpt1b, Cpt2, or the triple deletion of all three acyltransferases. We discovered that they display unique metabolic, physiological and molecular phenotypes. The loss of Cpt1a and Cpt1b or Cpt2 resulted in particular transcriptional outputs in hepatocytes. We show that much of the transcriptional signature is suppressed when deleting both Cpt2 and Ppara, showing the contribution of Ppara. Our results utilize stringent genetic mouse models to characterize the differential phenotypes of mice lacking Cpt1a and Cpt1b or Cpt2 and also show the contribution of a major transcription factor, Ppara.

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Vitamin B2 enables PPARa regulation of fasting glucose availability

Project description:Flavin adenine dinucleotide (FAD) mediates oxidation-reduction reactions required for cellular energy demands. Fatty acid oxidation (FAO) disorders caused by flavoprotein mutations and FAD depletion disrupt energy balance and glucose production during fasting. These FAO disorders are difficult to manage clinically, and their biochemical pathogenesis is poorly understood. Here, we identify a mechanistic connection between FAD levels and hepatic glucose production. Depleting the FAD pool in mice with a vitamin B2 deficient diet (B2D) resulted in phenotypes associated with organic acidemia phenotypes, including reduced body weight and whole-body fat oxidation rates coupled with hypoglycemia. Integrated discovery approaches revealed that B2D broadly tempered fasting activation of target genes for the nuclear receptor PPARa, including those required for gluconeogenesis. Consistent with this, Ppara knockout depleted liver FAD levels and worsened B2D hepatic glucose production. Treatment with the PPARa agonist fenofibrate overcame B2D phenotypes and rescued glucose availability and fatty liver signatures through activation of the integrated stress response and refilling anaplerotic amino acid substrates for glucose production. We conclude that PPARa governs metabolic responses to FAD availability and suggest pharmacologic activation as a strategy for treating disorders of riboflavin and FAD deficiency.

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Global hepatic gene expression data from PPARa liver KO, PPARa liver WT, PPARaKO and WT male mice treated or not with Fenofibrate

2016-02-20 | GSE73298 | GEO

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Project description:Fenofibrate is a specific agonist of the nuclear receptor PPARa. To identify the gene expression under the strict dependence of hepatic PPARa activity, we generated a new mouse strain of PPARa-specific deletion in hepatocyte (albumin-Cre+/- Pparaflox/flox or LKO) and we compared them to total Ppara KO (KO), wild-type (WT) and liver WT (albumin-Cre-/- Pparaflox/flox or LWT) mice. We used microarrays to detail the global programme of gene expression in liver of Ppara LKO, LWT, Ppara KO and WT male mice. There are 36 liver samples, each from an individual mouse. The samples are from Ppara liver KO (LKO), Ppara KO (KO), wild-type (WT) and liver WT (LWT) male mice of 14 week-old from the same genetic background (C57Bl/6J) treated with Fenofibrate (100 mg/kg/day) or vehicle (aqueous solution of gum Arabic 3%) by daily gavage for 10 days. n= 4 mice for LKO, LWT and WT genotypes treated with vehicle; n=3 for KO mice treated with vehicle; n=5 mice for LWT, LKO and KO genotypes treated with fenofibrate; n=4 WT mice treated with fenofibrate. All mice were sacrified at ZT14.

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2024-05-31 | GSE267915 | GEO

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