Liver perfusion experiments were performed to further investigate the origin of hypertriacylglycerolemia associated with endotoxemia in rats. For this purpose male rats were treated with E. coli endotoxin in a dose of 0.5 mg/100 g b.w. intravenously, deprived of food (with free access to water), and used 18 h later for liver perfusion experiments. Livers were isolated and perfused for 4 h with a medium consisting of Krebs-Ringer bicarbonate buffer containing bovine serum albumin (4%, w/v), glucose, 5 mM, oleate, 0.7-0.8 mM, and aged human erythrocytes, 20% (v/v). The rates of triacylglycerol (TAG) output, oleate uptake, and ketogenesis were measured. Endotoxin treatment did not induce changes of the rate of either TAG output or ketogenesis in the perfused liver. The data give further support to the contention that hypertriacylglycerolemia associated with endotoxicosis is unlikely to originate in an overproduction of TAG by the liver.