Brown adipose tissue (BAT) is present in most mammals and controls cold-induced and diet-induced thermogenesis. In rodents, BAT activation generates heat, dissipates excess energy and is required for survival. BAT is therefore considered a potential therapeutic target to increase energy expenditure (EE) and fight obesity. Until recently it has been thought that humans were devoid of functional BAT, questioning the relevance of rodent BAT metabolism to human obesity. However, the use of 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET) has revealed the presence of active depots of BAT in adult humans1-6. This has renewed scientific interest in understanding human BAT activation. BAT shares a common origin with skeletal muscle, supporting their common role in regulating metabolism and energy expenditure7. Human skeletal muscle-derived CD34+ brown adipocyte progenitor cells have also been identified8. These cells have increased uncoupled oxidative phosphorylation in vitro8 and an altered expression profile in obese patients9; they may potentially be another target to increase EE. The molecular mechanisms regulating human BAT and CD34+ brown adipocyte progenitor cells are not well established. MicroRNAs (miRNAs) are small regulatory molecules that regulate gene networks via their inhibition of protein translation or messenger RNA degradation10,11. A suite of mouse BAT-enriched miRNAs have been identified and several miRNA species can influence mouse brown adipocyte development in vitro12 13; whether these observations translate to human BAT is unknown. Here we present the miRNA profile of human BAT and differentiated human CD34+ brown adipocyte progenitor cells. Bioinformatics analysis has been used to identify miRNAs potentially involved human BAT development and function.