In the cold, the sympathetic nerves from the brain that innervate brown adipose tissue (Figure 1) are active and release norepinephrine (NE), which stimulates the brown fat cells. This leads to activation of triglyceride breakdown and intracellular release of fatty acids (FA). The fatty acids enter the mitochondria and are degraded through β-oxidation to acetyl-CoA (AcCoA), which enters the citric acid cycle (CAC). Stimulation of the cells by norepinephrine also leads to activation of UCP1, and this allows for the oxidative processes to proceed rapidly, uncoupled from ATP production, i.e., heat is produced. The method used by Ouellet et al. (2) (green) demonstrates increased metabolic activity in brown adipose tissue. A bolus of positron-labeled (¹¹C) acetate (*Ac^–) is injected into the blood and is converted within the cell to acetyl-CoA, which is incorporated into components of the citric acid cycle. When the citric acid cycle rapidly turns over, as happens in stimulated brown fat cells, the labeled carbons are released as CO₂, and the positron label is thus lost from the tissue in proportion to the metabolic activity of the tissue.