We study how liver metabolism is controlled at the molecular and organelle level, and how this control breaks down in metabolic disease. Our work focuses on hepatocyte-intrinsic mechanisms that integrate hormonal signals, nutrient availability, and microbiome-derived metabolites to regulate mitochondrial function

and metabolic flux. 
 

A central goal of the lab is to identify signaling pathways that directly remodel mitochondrial metabolism and quality control, thereby shaping gluconeogenesis, lipid handling, and nitrogen metabolism. By viewing hormones and metabolites as active drivers of intracellular metabolic state, rather than passive upstream cues, we define how hepatic metabolic capacity is dynamically tuned in health and disease.
 

Using primary hepatocytes, in vivo metabolic models, and multi-omic approaches, we aim to uncover fundamental principles governing hepatic metabolic flexibility and to identify new mechanistic targets relevant to metabolic liver disease

and type 2 diabetes.