Respiratory processes in brown adipose tissue.

These studies were initiated to ascertain whether, in rat brown adipose tissue as in white, lipolysis is a forerunner and fatty acid esterification an energy-consuming accompaniment of the increased oxygen uptake induced by catecholamines. No evidence could be obtained with brown adipose tissue slices to support this premise. Respiratory processes in homogenates of brown adipose tissue were therefore investigated. Oxygen consumption of homogenates of this tissue is increased about 25-fold upon the addition of a mixture of cofactors (coenzyme A, DL-carnitine, fumarate, and ATP). The addition of any single cofactor is without effect. The respiratory quotient of the process is less than 0.7. The stimulation of O2 consumption by cofactors is accompanied by a nearly go-fold increase in the yield of radioactive CO2 from added trace amounts of palmitate-lJ4C. Esterification of the added pahnitate to triglyceride occurs only when glycerophosphate is present in addition to cofactors. Addition of glycerophosphate without cofactors results in a IO-fold stimulation of oxygen consumption but has little effect on the conversion of added palmitate lW either to W02 or to triglycerides. It is concluded that, in the absence of glycerophosphate, addition of cofactors stimulates the oxidation of fatty acids present in the homogenate but not their esterification to triglyceride. Glycerophosphate oxidation is accompanied by the production of dihydroxyacetone phosphate and fructose 1,6diphosphate in amounts which account for the oxygen consumption observed. The oxidation of glycerophosphate is nearly completely inhibited by sodium cyanide and antimycin A, but is unaffected by the addition of sodium amytal, rotenone, or DPN. These results are interpreted to mean that oxidation of glycerophosphate is proceeding through the action of a DPN-independent glycerophosphate dehydrogenase. The addition of serum albumin (0.5%) to homogenates strongly inhibits the cofactor-stimulated O2 consumption, but has no effect on the oxidation of glycerophosphate. The results are discussed in relation to the production of high energy phosphate by brown adipose tissue.