Influence of parenteral carbohydrate on fat oxidation in surgical patients

The administration of parenteral carbohydrate to nutritionally depleted patients in amounts approximating energy expenditure will markedly suppress fat oxidation. If the amount of carbohydrate is increased, net lipogenesis will occur. In contrast, it has been reported that in acutely ill, hypermetabolic patients net fat oxidation continued during the administration of glucose in quantities that exceeded energy requirements. This investigation was undertaken in an attempt to determine to what extent the latter response is due to persistent oxidation of endogenous plasma free fatty acids (FFAs) or stores of lipid in tissue. In this study, carbohydrate intake above energy equilibrium resulted in a 29% increase in CO2 production, a 2% increase in O2 consumption, and an increase in respiratory quotient (RQ) from 0.77 to 0.97 in nutritionally depleted patients. Injured and infected patients displayed a 44% increase in CO2 production and a 15% increase in O2 consumption, while the RQ increased only to 0.9. An isotopic palmitate infusion was used to measure FFA oxidation during parenteral nutrition with variable amounts of carbohydrate. Simultaneous estimates of net fat oxidation were made by indirect calorimetry. At low carbohydrate intakes, oxidation of plasma FFAs accounted for 50% of net fat oxidation in both groups of patients. Suppression of FFA oxidation was greater in the nutritionally depleted patients than in the acutely ill group at intermediate and at high carbohydrate intakes. We conclude that the continued net fat oxidation seen in acutely ill patients receiving high carbohydrate intakes is at least partially due to continuing plasma FFA oxidation. Tissue fat stores that are not in rapid equilibrium with plasma FFAs make a substantial contribution to net fat oxidation.