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HGFAC is a ChREBP Regulated Hepatokine that Enhances Glucose and Lipid Homeostasis [RNA-Seq]

ABSTRACT: HGFAC is a ChREBP Regulated Hepatokine that Enhances Glucose and Lipid Homeostasis [RNA-Seq]

PROVIDER: PRJNA901514 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22288119_1.fastq.gz	Fastqsanger.gz
	SRR22288119_2.fastq.gz	Fastqsanger.gz
	SRR22288120_1.fastq.gz	Fastqsanger.gz
	SRR22288120_2.fastq.gz	Fastqsanger.gz
	SRR22288121_1.fastq.gz	Fastqsanger.gz

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HGFAC is a ChREBP Regulated Hepatokine that Enhances Glucose and Lipid Homeostasis [RNA-Seq]

Project description:Carbohydrate Responsive Element-Binding Protein (ChREBP) is a carbohydrate sensing transcription factor that regulates both adaptive and maladaptive genomic responses in coordination of systemic fuel homeostasis. Genetic variants in the ChREBP locus associate with diverse metabolic traits in humans, including circulating lipids. To identify novel ChREBP-regulated hepatokines that contribute to its systemic metabolic effects, we integrated ChREBP ChIP-seq analysis in mouse liver with human genetic and genomic data for lipid traits and identified Hepatocyte Growth Factor Activator (HGFAC) as a promising ChREBP-regulated candidate in mice and humans. HGFAC is a protease that activates the pleiotropic hormone Hepatocyte Growth Factor (HGF). We demonstrate that HGFAC KO mice have phenotypes concordant with putative loss-of-function variants in human HGFAC. Moreover, in gain- and loss-of-function genetic mouse models, we demonstrate that HGFAC enhances lipid and glucose homeostasis, which may be mediated in part through actions to activate hepatic PPARγ activity. Together, our studies show that ChREBP mediates an adaptive response to overnutrition via activation of HGFAC in the liver to preserve glucose and lipid homeostasis.

2022-11-15 | GSE217982 | GEO

HGFAC is a ChREBP Regulated Hepatokine that Enhances Glucose and Lipid Homeostasis [ChIP-Seq]

2022-11-15 | GSE217937 | GEO

HGFAC is a ChREBP Regulated Hepatokine that Enhances Glucose and Lipid Homeostasis

Project description:HGFAC is a ChREBP Regulated Hepatokine that Enhances Glucose and Lipid Homeostasis

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HGFAC is a ChREBP Regulated Hepatokine that Enhances Glucose and Lipid Homeostasis [ChIP-Seq]

Project description:HGFAC is a ChREBP Regulated Hepatokine that Enhances Glucose and Lipid Homeostasis [ChIP-Seq]

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HGFAC is a ChREBP-regulated hepatokine that enhances glucose and lipid homeostasis.

Project description:Carbohydrate response element-binding protein (ChREBP) is a carbohydrate-sensing transcription factor that regulates both adaptive and maladaptive genomic responses in coordination of systemic fuel homeostasis. Genetic variants in the ChREBP locus associate with diverse metabolic traits in humans, including circulating lipids. To identify novel ChREBP-regulated hepatokines that contribute to its systemic metabolic effects, we integrated ChREBP ChIP-Seq analysis in mouse liver with human genetic and genomic data for lipid traits and identified hepatocyte growth factor activator (HGFAC) as a promising ChREBP-regulated candidate in mice and humans. HGFAC is a protease that activates the pleiotropic hormone hepatocyte growth factor. We demonstrate that HGFAC-KO mice had phenotypes concordant with putative loss-of-function variants in human HGFAC. Moreover, in gain- and loss-of-function genetic mouse models, we demonstrate that HGFAC enhanced lipid and glucose homeostasis, which may be mediated in part through actions to activate hepatic PPARγ activity. Together, our studies show that ChREBP mediated an adaptive response to overnutrition via activation of HGFAC in the liver to preserve glucose and lipid homeostasis.

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HGFAC is a ChREBP Regulated Hepatokine that Enhances Glucose and Lipid Homeostasis

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

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PHLPP1 promotes lipid accumulation through AMPK/ChREBP dependent lipid uptake and fatty acid synthesis pathway

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Proline hydroxylation of ChREBP

Project description:This project investigated proline hydroxylation of ChREBP. Proline hydroxylation was investigated in flag-IP enriched protein extracts from ChREBP-flag overexpressing HEK293 cells (A) and in ChREBP-IP enriched mouse liver protein (male, C57BL6/J) (B).

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Integrative genomics outlines a biphasic glucose response and a ChREBP-RORÎ³ axis regulating proliferation in Î²-cells

Project description:Glucose is an important regulator of pancreatic Î²-cell function. In addition to the acute stimulation of insulin secretion, glucose stimulates long-term adaptive changes in gene expression that can either promote or antagonize the proliferative potential and function of Î²-cells. The glucose-sensing transcription factor carbohydrate response element binding protein (ChREBP) has been shown to promote both Î²-cell proliferation and dysfunction; however, the molecular mechanisms underlying these pleiotropic effects of ChREBP and glucose are not well understood. Here, we have generated time-resolved profiles of enhancer and transcriptional activity in response to glucose in the INS-1E pancreatic Î²-cell line. Our data outline a biphasic response with a first wave during which metabolic genes are activated, and a second wave where cell cycle genes are induced and Î²-cell identity genes are repressed. We show that ChREBP directly activates first wave genes, whereas repression and activation of second wave genes by ChREBP is indirect. By integrating motif enrichment within late-regulated enhancers with expression profiles of the associated transcription factors, we identify multiple putative regulators of the second wave, including RAR-related orphan receptor (ROR) Î³, which we demonstrate is a novel direct ChREBP target gene. Importantly, we show that RORÎ³ activity is necessary for full glucose-induced proliferation of both INS-1E and primary rat Î²-cells. Genome-wide assesment of the transcriptional response to glucose in INS-1E Î²-cells using RNA- ChIP- and DNase-seq

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