Key result
HGFAC knockout raises circulating triglycerides by ~39% and impairs glucose tolerance in mice.
Why the study?
ChREBP regulates systemic fuel homeostasis and genetic variants in its locus associate with metabolic traits, but novel ChREBP-regulated hepatokines contributing to these effects remain to be identified.
Absolute Event Rate: 100% vs 72%
p-value: p=<0.001
HGFAC is identified as a novel ChREBP-regulated hepatokine that preserves glucose and lipid homeostasis through an HGFAC-HGF-PPARγ signaling axis.
Animal findings nominate HGFAC as a metabolic hepatokine; leaves open human translation and therapeutic targeting.
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, in part, through actions to activate hepatic PPARγ activity. Together, our studies show that ChREBP mediates an adaptive response to overnutrition via activation of an HGFAC-HGF-PPARγ signaling axis in the liver to preserve glucose and lipid homeostasis.
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Sargsyan et al. (2021) studied Metabolic homeostasis. HGFAC knockout vs. Wild-type controls was evaluated on Circulating triglycerides (mg/dl) (p=<0.001). HGFAC knockout in mice increased circulating triglycerides by 28% (100 vs 72 mg/dl) and impaired glucose tolerance, demonstrating its role in preserving glucose and lipid homeostasis.
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