Effect of thermal injury on relative anaplerosis and gluconeogenesis in the rat during infusion of [U-13C] propionate

A new approach for the analysis of hepatic metabolism after burn injury is introduced. Relative anaplerotic, pyruvate recycling and gluconeogenic fluxes were measured by 13C NMR isotopomer analysis of blood glucose from rats with 40% body surface area injury, and from rats exposed to sham injury. A short chain fatty acid, [U-13C] propionate which is avidly extracted by the liver, was infused intravenously to deliver 13C into the citric acid cycle. There was no difference in the multiplets detected in the glucose carbon-2 (C-2) anomer from blood or liver after 45 or 60 min of infusion of propionate, indicating that steady-state isotopic conditions were achieved. Gluconeogenesis relative to citric acid cycle flux was not altered by burn injury; in both sham and burn groups the rate of glucose production was about equal to flux through citrate synthase. In the sham group of animals the rate of entry of carbon skeletons into the citric acid cycle was about four times citric acid cycle flux in animals after thermal injury. Similarly, flux through pyruvate kinase (again relative to citrate synthase) was significantly increased in burn injury.