Brown adipose tissue (BAT) functions as an energy expenditure organ through facilitating adaptive thermogenesis in the body. The process occurs in mitochondria where UCP-1 uncouples oxidative phosphorylation in aerobic respiration which causes loss of protons and leads to the generation of heat instead of ATP. Activation of BAT allows increasing energy expenditure and improving weight control. Therefore, since the rediscovery of metabolically active BAT in adults, it’s targeting/activation has been suggested to combat metabolic diseases like diabetes and cardiovascular diseases. One approach has been adiponectin replacement therapy which has given contradictory findings regarding adiponectin’s effects in BAT. Therefore, the current project studied BAT structure and function in APNtg mice with elevated levels of adiponectin. Results showed larger tissue in APNtg mice compared to control mice which should indicate improvement in energy homeostasis. This was studied through morphology findings via different stainings and RT-PCR, and mitochondrial activity via UCP-1 protein expression. All results in the current study indicated disruption of enlarged BAT structure in APNtg mice, which could hinder healthy tissue growth and lead to metabolic challenges inside the tissue. Problems with BAT functionality was shown to be compensated through browning and increased mitochondrial activity in white adipose tissue in response to cold-exposure. In conclusion, the current study proposes that enlarged BAT in APNtg mice is not fully functional and the need for thermoregulation might enhance browning and beige cell activation in white adipose tissue in these mice.