Mitochondrial energy metabolism is critical for life and altered metabolism is associated with many disease states. Our lab is particularly focused on regulation of mitochondrial number and function during disease. Utilizing mouse models of insulin resistance and diabetes we study the effects of excess circulating fatty acid on energy metabolism.

In addition we are developing projects aimed at understanding how alterations in the environment of developing organisms may reprogram mitochondria and predispose to risk of disease later in life. Epidemiologic data demonstrates that a variety of environmental insults during development (intrauterine growth retardation, infants of diabetic mothers) predispose to diseases such as diabetes and heart disease. We plan to use drosophila as a genetic model to probe the mechanistic basis of these changes, with a particular focus on mitochondria.

Mitochondrial energy metabolism is critical for life and altered metabolism is associated with many disease states. Our lab is particularly focused on regulation of mitochondrial number and function during disease. Utilizing mouse models of insulin resistance and diabetes we study the effects of excess circulating fatty acid on energy metabolism.

In addition we are developing projects aimed at understanding how alterations in the environment of developing organisms may reprogram mitochondria and predispose to risk of disease later in life. Epidemiologic data demonstrates that a variety of environmental insults during development (intrauterine growth retardation, infants of diabetic mothers) predispose to diseases such as diabetes and heart disease. We plan to use drosophila as a genetic model to probe the mechanistic basis of these changes, with a particular focus on mitochondria.