Pharmacological Sparing of Protein in Burn Injury
TEXAS UNIV MEDICAL BRANCH AT GALVESTON
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We have investigated the responsiveness of protein kinetics to insulin and the role of glucose oxidation rate as a mediator of the protein catabolic response to burn injury and sepsis by assessing the response of leucine and urea kinetics to a 5 hour hyperinsulinemic euglycemic clamp with and without the simultaneous administration of dichloroacetate DCA, to further increase glucose oxidation via stimulation of pyruvate dehydrogenase activity in 8 severely burned and 8 septic patients. Leucine and urea kinetics were measured. Compared to controls, basal leucine kinetics flux and oxidation were significantly elevated in both groups of patients. Hyperinsulinemia elicited significant decreases in leucine kinetics in both groups of patients. The administration of DCA to patients during hyperinsulinemia elicited a significant increase in glucose oxidation rate and the percent of glucose uptake oxidized increased yet the response of leucine and urea kinetics to the clamp plus DCA was not different from the response to the clamp alone. These results suggest that the maximal effectiveness of insulin to suppress protein breakdown is not impaired and that a deficit in glucose oxidation or energy supply is probably not playing a major role in mediating the protein catabolic response to severe burn injury and sepsis.