A high-protein meal exceeds anabolic and catabolic capacities in rats adapted to a normal protein diet

Citation
C. Morens et al., A high-protein meal exceeds anabolic and catabolic capacities in rats adapted to a normal protein diet, J NUTR, 130(9), 2000, pp. 2312-2321
Citations number
42
Categorie Soggetti
Food Science/Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF NUTRITION
ISSN journal
00223166 → ACNP
Volume
130
Issue
9
Year of publication
2000
Pages
2312 - 2321
Database
ISI
SICI code
0022-3166(200009)130:9<2312:AHMEAA>2.0.ZU;2-0
Abstract
The postprandial fixation of dietary nitrogen in splanchnic and peripheral tissues as well as its dynamic transfer to the nitrogen pools of the body w ere quantified in rats subjected to an acute augmentation of dietary protei n. For this purpose, we traced the dietary protein and studied the immediat e fate of exogenous nitrogen in many tissues and biological fluids. Rats we re adapted to a diet providing an adequate protein level (14 g/100 g), and then fed a meal containing either 0.42 g (Group A) or 1.50 g (Group H) of [ N-15]-labeled milk protein. The amounts of exogenous nitrogen transferred t o urea (0.32 +/- 0.04 vs. 2.46 +/- 0.25 mmol, respectively), incorporated i n splanchnic (0.41 +/- 0.02 vs. 0.87 +/- 0.10 mmol) and peripheral (1.65 +/ - 0.84 vs. 2.36 +/- 0.49 mmol) tissue protein were higher in group H than i n group A. Individual plasma amino acids (AA) [N-15]-enrichments showed tha t AA respond differentially to an acute augmentation of dietary intake. Thi s work provides new descriptive and quantitative information on the metabol ic fate of dietary nitrogen in the postprandial state. It highlights the hi gher integration of a surplus of dietary nitrogen in the tissues even if it is rapidly limited by saturation of the protein synthesis capacities. The main metabolic response remains the stimulation of AA degradation, leading to a large rise in urea production. However, both anabolic and catabolic sy stems are exceeded, resulting in an elevation of peripheral AA and negative feedback on the gastric emptying rate.