Brown fat physiology has been of considerable interest recently in the context of metabolic disease. Brown fat can synthesize and store lipids, and rapidly burn stored lipids to generate heat. The former is an ATP-consuming process referred to as de novo lipogenesis. Recent evidence supports the idea that mild cold acts predominantly through the sympathetic nervous system to stimulate de novo lipogenesis, even as it stimulates lipolysis and fatty acid ß-oxidation. This effect, which is mediated by the mTORC2-Akt2 signaling module, is thought to optimize fuel storage and thermogenesis. In contrast to mild cold, severe cold directly cools brown fat tissue and inhibits mTORC2, overriding ß-adrenergic stimulation mediated by Gs protein. The consequent inhibition of mTORC2-Akt2 signaling blocks activation of ATP citrate lyase, a key enzyme in de novo lipogenesis. We propose the novel view that this cell-autonomous effect on brown fat is in service of defending core temperature by channeling metabolic activity away from ATP-dependent de novo lipogenesis and exclusively towards lipolysis/ß-oxidation and thermogenesis. Thus, direct effects of cold act in concert with ß-adrenergic-mediated effects to generate non-linear both catabolic and anabolic responses of brown fat to progressive cold. The goal of this collection is to demonstrate standardized protocols on mTOR signaling and brown fat metabolism.