Brown adipose tissue is thermogenically active when coupling of oxidative phosphorylation is loosened. Brown‐adipose‐tissue mitochondria when freshly isolated are uncoupled. They are brought to a coupled state by oxidation of endogenous fatty acids, after which addition of exogenous fatty acids produces a burst of oxygen consumption. This does not correspond to that theoretically required for complete oxidation of the added fatty acid to carbon dioxide and water. Oxidation by coupled mitochondria of 14C‐labelled palmitic acid in the presence of malate leads to labelling of water‐soluble intermediates. These intermediates are identified as citric acid cycle intermediates, amino acids arising from transamination, and acetyl L‐carnitine. It is found that in coupled and uncoupled conditions the ratio of acetyl L‐carnitine to other intermediates is altered. Uncoupling reduces the formation of acetyl L‐carnitine and increases entry of acetyl groups into the citric acid cycle. A control mechanism for this process and its possible correlation with the physiological function of brown adipose tissue are discussed.