I am a physician-scientist independently directing a basic science research laboratory that studies the connection between adipose tissue and infection. We use mouse models to understand the role of adipose tissue as a source of signaling molecules called adipokines and as a substrate for generation of ATP and biomolecules in the response to infection, especially influenza.

During my PhD, I studied intermediary metabolism using stable isotope tracing in combination with gas/liquid chromatography and mass spectrometry. My main project involved determining the metabolic pathways that cells use for growth when deprived of pyruvate dehydrogenase.  Understanding cellular metabolism and carbon flux prepared me conceptually for my work in the Friedman Lab, where metabolic dysregulation in obesity is examined on an organismal scale.  After my residency in Internal Medicine and my Pulmonary/Critical-care Fellowship at Columbia University, I started my post-doctoral fellowship in the Lab of Jeffrey Friedman at Rockefeller University. My primary research interest was to understand the role of leptin signaling in influenza infection. To accomplish this project, we collaborated with Dr. Diane Mathis of Harvard University, an immunologist who studies the host response in the context of metabolic disease. We discovered that leptin is crucial for surviving influenza infection but it’s role in increasing survivability is surprisingly not due to better immunological control of the virus. Our findings are discussed in a manuscript recently published in The Journal of Clinical Investigation. Future studies are focused on understanding this mechanism.

The other part of my laboratory is devoted to understanding how adipose tissue can be used as a fuel during infection. We have some interesting preliminary data that upregulating lipolysis protects mice from LPS-induced inflammation. Current studies are focused on understanding the mechanism underlying this phenomenon and the fate of the fatty acids and glycerol that are liberated from adipose tissue. Carnitine palmitoyltransferase Ia (CPT1a) is the rate limiting step of mitochondrial long chain fatty acid oxidation (FAO). We are using mouse models of tissue specific CPT1a deficiency in combination with metabolomics to understand the role to define the role of FAO in the response to infection.