title: Effect of severe burn injury on substrate cycling by glucose and fatty acids.
abstract: Increases in metabolic rate and core temperature are common responses to severe injury. We have investigated the hypothesis that these responses are due to increases in substrate cycling. A substrate cycle exists when opposing, nonequilibrium reactions catalyzed by different enzymes are operating simultaneously. At least one of the reactions must involve the hydrolysis of ATP. Thus, a substrate cycle both liberates heat and increases energy expenditure, yet there is not net conversion of substrate to product. In studies in volunteers (n = 18) and in patients with severe burns who were in a hypermetabolic state (n = 18), we used stable-isotope tracers to quantify substrate cycling in the pathways of glycolysis and gluconeogenesis and a cycle involving the simultaneous breakdown and synthesis of stored triglyceride (triglyceride-fatty acid cycle). The total rates of triglyceride-fatty acid and glycolytic-gluconeogenic cycling were elevated in the patients by 450 and 250 percent, respectively (P less than 0.01). An infusion of propranolol in the patients greatly reduced triglyceride-fatty acid cycling but did not affect gluconeogenic-glycolytic cycling. We conclude that increased substrate cycling contributes to the increased thermogenesis and energy expenditure following severe burns and that the increased triglyceride-fatty acid cycling is due to beta-adrenergic stimulation.
mesh_terms: D000293:Adolescent; D000328:Adult; D001833:Body Temperature Regulation; D002056:Burns / Q000378:metabolism* / Q000503:physiopathology; D002648:Child; D002675:Child, Preschool; D004734:Energy Metabolism; D005227:Fatty Acids / Q000378:metabolism*; D005943:Gluconeogenesis; D005947:Glucose / Q000378:metabolism*; D006019:Glycolysis; D006801:Humans; D011433:Propranolol / Q000494:pharmacology; D014280:Triglycerides / Q000378:metabolism
chemical_list: D005227:Fatty Acids; D014280:Triglycerides; D011433:Propranolol; D005947:Glucose