ARE LEUCINE TURNOVER MEASUREMENTS VALID IN THE INTRAVENOUSLY FED STATE

We tested whether the primary or reciprocal pool models for whole-body leucine kinetics accurately depict human adaptation to protein defici ency and repletion in the fed state by comparing model derived leucine oxidation with urea appearance calculated from urinary urea excretion and changes in the body urea pool. Five normal men consumed a control diet providing maintenance energy and 80 g protein/d for 5 days; this was followed by 7 days of an isoenergetic protein-free diet, and fina lly by a return to the original control diet for 5 days. At the end of each dietary period, urea appearance and leucine oxidation were measu red during a 4-hour intravenous infusion of crystalline amino acids pr oviding a total N to leucine N ratio similar to that in mixed body pro teins. Primary pool-derived fed-state leucine oxidation decreased afte r adaptation to protein deficiency and remained low during refeeding ( 18.6 +/- 1.2, 13.2 +/- 1.1, and 15.0 +/- 1.8 mu mol.kg(-1).h(-1), resp ectively, P < .01), in agreement with the physiologic prediction. A si milar pattern occurred with the reciprocal pool model (24.4 +/- 2.7, 1 7.3 +/- 2.0, and 20.3 +/- 2.7 mu mol.kg(-1).h(-1), P < .01) as well as with urea N appearance (3.06 +/- 0.32, 2.34 +/- 0.24, and 2.38 +/- 0. 26 mmol N.kg(-1).4 h(-1) P < .05). Despite these relative agreements, absolute rates of whole-body amino acid oxidation were 25% (reciprocal pool model) to 43% (primary pool model) lower than when estimated fro m urea N appearance. Thus, although both intravenously fed-state leuci ne turnover models accurately depicted the pattern of changes in whole -body protein oxidation after adaptation to protein deficiency and dur ing repletion, there is some evidence that they underestimated the tru e leucine oxidation rate. Copyright (C) 1994 by W.B. Saunders Company