Herman Award Lecture, 1996: relation of metabolic studies to clinical nutrition--the example of burn injury.
The optimal nutritional support of critically ill patients should be based on the metabolic response. Therefore, we performed a series of experiments in patients using stable isotopic tracers designed to elucidate the responses of glucose, fatty acids, and protein metabolism in severely burned patients. Glucose production was elevated above normal as a result of an increase in glucagon concentration. The peripheral hypoglycemic action of insulin was diminished, as was its effectiveness in suppressing endogenous glucose production, but the intracellular capacity to oxidize glucose was not impaired. Lipolysis was stimulated by beta 2-adrenergic stimulation to a much greater extent than was fatty acid oxidation, with the result being an increase in the recycling of fatty acids secreted in very-low-density lipoproteins. Muscle protein catabolism was accelerated in severely burned patients, leading to a progressive loss of lean body mass that was not prevented by nutritional support alone. The ineffectiveness of nutritional support for muscle was due to alterations in amino acid transmembrane transport kinetics that favored efflux. Treatment with exogenous insulin stimulated inward amino acid transport and muscle protein synthesis. Extrapolation from our current knowledge of metabolism to clinical treatment indicates that nonprotein energy should be provided largely in the form of carbohydrate. If hyperglycemia ensues, exogenous insulin will further increase the anabolic response in muscle. Protein requirements can be met with 1.5 g protein.kg-1.d-1. Treatment with anabolic hormones may ultimately be the most effective way in which to optimize the response to nutritional support.
Department of Surgery, University of Texas Metabolism Branch, Shriners Burns Institute, Galveston 77550, USA.
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D001363:Awards and Prizes; D002056:Burns / Q000178:diet therapy / Q000378:metabolism*; D004035:Diet Therapy / Q000592:standards*; D005227:Fatty Acids / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000494:pharmacology; D050356:Lipid Metabolism; D009124:Muscle Proteins / Q000378:metabolism*; D010084:Oxidation-Reduction; D012955:Societies, Medical; D014481:United States
D005227:Fatty Acids; D007328:Insulin; D009124:Muscle Proteins; D005947:Glucose