As a member of the Molecular Carcinogenesis and Chemoprevention Program at the OSUCCC – James, I am interested in the study of whole-body energy metabolism as regulated by interactions between adipose, liver and muscle tissues.

Canonical mechanisms of energy metabolism involve insulin-dependent and -independent pathways in each of these tissues. In addition, adipose secretes adipokines that regulate metabolism and inflammation in non-adipose tissues. My lab team seeks to understand how the availability or lack of availability of energy substrates and bioactive compounds (e.g., adipokines and dietary components) modulate metabolism and function of adipose and muscle tissues.

Energy deprivation induces atrophy of muscle and adipose using some overlapping mechanisms, including altered metabolism, inflammation, proteolysis and cell death-associated signals. My work with muscle involves identifying the steps of atrophy related to insulin resistance, proteolysis and cell death by using a murine model of muscle atrophy that is induced by cancer cachexia. In this mouse model, cachexia appears to involve early alterations of insulin-mediated metabolism and inflammation that contribute to diminished energy substrate and compromised function of skeletal muscle.