A rat model for evaluating leucine oxidation after skeletal trauma

The oxidation of branched-chain amino acids following skeletal trauma or sepsis is considered a crucial event in the protein wastage that accompanies these stresses. This investigation undertook to monitor changes in leucine oxidation following bilateral femoral fracture to the rat to determine if this model is appropriate for monitoring specific amino acid oxidation after trauma. Thirty-five rats had hindlimb fractures and were fed an oral liquid diet ad libitum; 35 healthy rats were pair-fed with the trauma group. Food intake, body weight, and urinary nitrogens were monitored daily for all rats, and leucine oxidation was measured for five rats from each group on days 1 through 7 post-trauma. Leucine oxidation was qualitatively compared between the groups (from the percentage of isotope respired in 4 hours following a single injection of L-[l-14C] leucine). Skeletal fracture resulted in increased urinary nitrogen excretions on days 2 through 5 when compared to pair-fed animals. The traumatized rats compared to pair-fed controls had elevated leucine oxidation on days 2 through 4, and a tendency towards elevation on day 5. The peak in elevation occurred on day 3 when leucine oxidation was increased 49% above pair-fed rats. The data suggest an association between leucine oxidation and urinary excretion of nitrogen in this trauma model, and when the results are compared to our previous studies of leucine oxidation in traumatized patients, traumatized rats appear to respond similarly to injured patients in the acceleration of leucine oxidation.