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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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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

| PRJNA901511 | ENA

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]

| PRJNA901431 | ENA

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

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

2022-11-15 | GSE217983 | GEO

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

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

| PRJNA795062 | ENA

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

2016-09-06 | E-GEOD-81628 | biostudies-arrayexpress

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).

2020-10-19 | PXD019137 | Pride

Intergrated expression profiling and ChIP-SEQ analyses of ChREBP-mediated glucose response network (expression data only)

Project description:We identified ChREBP-binding regions from the DNA of human hepatocellular targets as well as previously-known targets Total RNA from hepG2 cell line

2010-06-16 | E-GEOD-22074 | biostudies-arrayexpress

Activation of skeletal ChREBP increases IMFlevel in mice and Broiler Chickens

Project description:Intramuscular fat (IMF) content is one of the key factors affecting meat quality. Carbohydrate response element binding protein (ChREBP) can promote glucose metabolism and fat synthesis by activating the expression of glycolysis and lipogenesis-related genes, but its function and regulatory mechanism in IMF are still unclear. This study evaluated the correlation between TG content and ChREBP expression level in muscles of different species to reveal the relationship between ChREBP and IMF. RNA-seq analysis showed that overexpressing ChREBP in C2C12 cells can significantly up-regulate fatty acid synthesis pathways, while significantly down-regulate the expression levels of muscle development pathways and related genes. In vivo, we found that overexpression of ChREBP or activation by fructose significantly increased the triglyceride content of the tibialis anterior muscle (TA) and the IMF content of yellow feather chicken leg and breast muscle in mice. And lipidomics data also found that feeding fructose can change the lipid composition of yellow feather broiler breast muscle and improve the flavor substances. This study demonstrated that ChREBP is a key gene regulating IMF deposition, providing a new target for genetic selection and nutritional regulation of IMF content.

2024-08-08 | GSE228899 | GEO

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