Mitochondria are the major site for fuel oxidation in cells and strategies that stimulate mitochondria to burn more calories may prove beneficial for preventing obesity and insulin resistance. Recently it has emerged that post-translational modification of proteins in mitochondria can have major effects on the rate of fuel oxidation. This project will use both genetic and pharmacological approaches to alter post-translational modifications (e.g. lysine acetylation – Ac -K) in mitochondrial proteins and examine the effect on lipid accumulation and insulin action.