We use mouse models to deconstruct how energy is regulated during infection. We seek to translate these studies into identifying therapeutic strategies for the human response to infection. Equally important, our goal is to train the next generation of biomedical scientists and physicians, both for academics and industry.


Energy regulation is a highly integrated process that relies on signaling from the periphery to the brain to control behaviors like locomotion and food intake and demanding physiological processes like reproduction and immune function.  Energy is stored as adipose tissue which is catabolized to release free fatty acids and glycerol during energy deficits.  Infection is a particularly stressful condition: the immune response increases energetic demands while at the same time inducing anorexia which reduces energy intake.  Various humoral and neural signals mediate the mobilization of fat stores to meet energy needs but the precise mechanisms that are operative during infection are poorly understood.  While “the obesity paradox” asserts that increased adipose tissue can be protective during critical illness, extensive epidemiologic data shows increased mortality in respiratory viral infection at high BMI.  This suggests that adipose tissue can be both protective and deleterious based on context.  Our group studies the role of adipose tissue during infection to critically evaluate its role in outcomes.  To address this, we use mouse models of dysregulated energy metabolism to uncover the role that fat plays in the response to infection on a systems level.  By understanding how adipose tissue shapes the response to infection, we hope to optimize nutrition during infection as well as discover possible therapeutic targets for vulnerable populations.