Rapidly emerging functions and areas of study in BAT biology incite multiple tissues and processes. For example, neuronal and immune signaling exert a regulatory effect on brown fat cells, cold temperatures induce de novo brown adipocyte differentiation, and substrates beyond glucose can fuel thermogenesis. Brown fat cells also exert control over endocrine functioning and show heterogeneity with specific metabolic activity. Moreover, WAT can respond to cold temperatures by remodeling to a BAT-like phenotype. While UCP1 generates heat by disruption of the mitochondrial inner membrane electrochemical gradient, UCP1-independent mechanisms that fueling adipocyte thermogenesis also exist. Understanding the interplay between these systems may lead to strategies for harnessing the power of BAT in the treatment for human metabolic disease.