Objective：The aim of this study was to investigate the role of curcumin in promoting browning of white adipocytes and its underlying mechanisms through in vitro experiments. Methods：The subcutaneous primary adipocytes were extracted from mice and induced to differentiate into mature. Intervention with different concentrations of curcumin（10，20，40 μmol/L）for 48 h. Lipid droplet morphology was observed by oil red O staining. Intracellular mitochondria were detected with mitochondrial green fluorescent probe（Mito Tracker Green）. Mitochondrial superoxide indicator（Mito SOX Red） was used to determine the level of mitochondrial reactive oxygen species（ROS）. Intracellular ATP content was detected by the ATP assay kit. The expression of the browning-related marker gene was detected by real-time PCR. Finally，the mechanism was explored by using β3 adrenergic receptor（β3-AR） antagonist（SR59230A）. Results：In mouse subcutaneous primary adipocytes，curcumin markedly alleviates intracellular lipid accumulation. And more mitochondria were observed after curcumin treatment（P < 0.001）. Otherwise，curcumin of low dose（10，20 μmol/L） also reduced the production of ROS（P < 0.01），but increased the intracellular ATP content（P < 0.05）. In addition，curcumin can up-regulate the mRNA expression of the brown fat marker genes［β3-AR，uncoupling protein 1（UCP1），PPARγ coactivator-1α（PGC1α）］（P < 0.05）. However，β3-AR antagonist can antagonize the function of curcumin. Conclusion：Curcumin has the potential to promote mitochondrial biogenesis，improve their function and evoking white adipocyte browning through regulating β3-AR-dependent signaling pathway.