We and others have recently shown that myoglobin (MB) is highly expressed in brown adipose tissue (BAT), where its expression increases with brown adipocyte differentiation and furthermore with BAT activation in vivo [1]. We show that expression levels of MB in brown and white adipocytes control mitochondrial respiratory capacity and increase the acute response to adrenergic signaling and lipolysis. We were the first to demonstrate MB’s interaction with lipids as the mode of action underlying increased respiration using non-lipid binding MB mutants. 

Together with our collaborators at the Helmholtz Center for Environmental Research (UFZ), we are currently establishing metabolomics approaches to assess MB effects on intracellular substrate fluxes and further investigate the effects of MB on energy expenditure in conditionally altering MB gene expression in adipose tissues in mice.