Metabolic response to burn injury: nutritional implications

Abstract

The response to critical illness involves alterations in all aspects of metabolic control, favoring catabolism of stored energy substrates and protein. Glucose production is accelerated, due principally to a chronic elevation in glucagon. Whereas glucose is available at increased rates, the muscle tissue is less responsive than normal to the stimulatory effect of insulin on glucose uptake. Stored triglyceride is also catabolized at a high rate, predominantly due to enhanced adrenergic activity. This causes the release of free fatty acids at a rate well in excess of their requirement for oxidation, leading to a high rate of reesterification and triglyceride transport in plasma. Protein metabolism is characterized by accelerated catabolism that is not balanced by a corresponding increase in synthesis. Whereas the mechanism for this response is not known, peripheral insulin resistance does not appear to be responsible.