Research
Our lab studies how intracellular signaling pathways
and mitochondria control hepatic metabolism
in physiology and metabolic disease.
The research projects below explore this problem
from complementary experimental
and conceptual perspectives.
Chemokine Control
of Liver Metabolism
Chemokines are best known for their roles in immune cell trafficking, but we study how chemokine receptors directly
regulate hepatocyte metabolism.
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We examine non-canonical chemokine signaling pathways in the liver and how they influence lipid handling,
mitochondrial function,
and metabolic flexibility.
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By viewing chemokine receptors as metabolic signaling nodes rather than inflammatory markers, we define a new interface between immune-derived cues and intrinsic hepatic metabolic control
in metabolic liver disease.
Microbiome-Derived Metabolites and Liver Metabolism
Gut microbiota-derived metabolites are increasingly recognized as regulators of host physiology, and we study how they directly shape hepatocyte metabolic state.
We examine how microbial metabolites, particularly indole derivatives, modulate hepatic glucose production, mitochondrial metabolism, and metabolic flexibility.
By linking microbiome-derived chemical signals to intrinsic hepatocyte metabolic control, this work defines a direct mechanistic bridge between the gut microbiome and liver metabolism in metabolic disease.
Hormonal Regulation of Mitochondrial Function
We study how hormonal signals, particularly glucagon, remodel mitochondrial function to control
hepatic metabolic output.
This work examines how hormone-driven signaling pathways regulate mitochondrial organization, metabolic flux, and quality control in hepatocytes, integrating pathways that span energy metabolism
and nitrogen handling.
By defining mitochondria as dynamic effectors of hormonal signaling rather
than static metabolic engines, this research reveals how endocrine cues reprogram liver metabolism in health
and metabolic disease.