In vivo demonstration of nitrogen-sparing mechanisms for glucose and amino acids in the injured rat.

Changes in protein metabolism 8 hr after anesthesia and femur fracture were studied in healthy rats fasted or receiving either intravenous glucose or crystalline amino acids. Whole body rates of amino acid turnover (flux) and release from protein (breakdown) as well as fractional synthetic rates of mixed muscle, liver, and plasma protein were measured using the constant infusion of L-(I-14C)-leucine. Injury resulted in a 24% increase in the synthesis of liver (p less than 0.05) and plasma proteins (p less than 0.01), respectively. Amino acid infusions in the injured animals further increased the synthesis of liver protein (from 36.6% to 44.3%/day, p less than 0.05) and increased muscle protein synthesis (from 7.0% to 9.3%/day, p less than 0.05) without altering rates of protein breakdown. Glucose infusions, in contrast, reduced whole body protein breakdown 36% (p less than 0.05) when compared to fasting, and depleted the plasma essential amino acid pool (p less than 0.05). The usual increases in liver protein synthesis observed in fasted rats following injury were not seen when the animals were receiving intravenous glucose. The nitrogen-sparing mechanism of these two infusions are different. Protein-free glucose infusions impair the normal response to injury aimed at increasing visceral protein synthesis and maintaining plasma essential amino acid concentrations.