Adipocytes are unique multifunctional cells central to control of energy homeostasis. Among their important functions is the storage of excess nutrients as neutral lipids, primarily triglycerides. These lipid stores can be mobilized in times of need. Activation of the sympathetic nervous system promotes energy mobilization in adipocytes via the secretion of catecholamines from sympathetic nerve terminals in the adipose tissue. Subsequent b-adrenergic signaling stimulates adipocyte lipolysis, whereby triglycerides are broken down to glycerol and free fatty acids that are utilized as an energy source throughout the body. Interestingly, one to two thirds of the secreted fatty acids are taken back up by the adipocytes themselves. These fatty acids either undergo a futile cycle of re-esterification or alternatively mitochondrial b-oxidation. Interestingly, b-adrenergic stimulation of adipocytes appears to favor oxidation. Dr. Reilly discovered that this change in fatty acid deposition in lipolytic adipocytes is due to a blockade of re-esterification, thus diverting fatty acids towards oxidation. Interestingly, this process requires the activation of STAT3, which suppresses the activity of GPAT3, the rate limiting enzyme in fatty acid esterification. Furthermore, lipolysis-driven oxidative metabolism significantly impacts whole body energy balance and the development of diet-induced obesity. Dr. Reilly continues to investigate the molecular pathways regulating lipolysis-driven respiration and their role in adipocyte energy balance and obesity. These efforts could lead to the identification of new therapeutic targets in the fight against obesity.