DISCRIMINATION OF NITROGEN ISOTOPES DURIN G LIVER-METABOLISM FEEDING DIFFERENT FOOD PROTEINS

Citation
H. Sick et al., DISCRIMINATION OF NITROGEN ISOTOPES DURIN G LIVER-METABOLISM FEEDING DIFFERENT FOOD PROTEINS, Isotopenpraxis, 30(2-3), 1994, pp. 111-121
Citations number
13
Categorie Soggetti
Chemistry Inorganic & Nuclear","Nuclear Sciences & Tecnology
Journal title
ISSN journal
00211915
Volume
30
Issue
2-3
Year of publication
1994
Pages
111 - 121
Database
ISI
SICI code
0021-1915(1994)30:2-3<111:DONIDG>2.0.ZU;2-B
Abstract
Nitrogen isotope ratio disproportionation (N-IRD) is the result of iso tope effects of different magnitude in branched pathways of nitrogen m etabolism of the liver. N-IRD is measured as the difference of natural N-15 abundance of urea and plasma protein and is noted in parts per t housand (per mill) as the difference of their delta values. It was der ived that N-IRD would become maximum if the amino acid pattern consume d by the respective pathways urea synthesis and protein synthesis of t he liver is identical. This is expected if the metabolic available ami no acid pattern exactly meets requirement. When feeding rats methionin e(met)-supplemented casein N-IRD increased from 6 parts per thousand a t zero protein intake to 8 parts per thousand at the requirement intak e of 5 g/kg BM())/day. With further increasing protein intake N-IRD d ecreased to values below 6 parts per thousand. It was concluded that i ncreasing N-IRD with increasing intake of met-supplemented casein is c aused by complementation of the endogenous amino acid pattern by exoge nous dietary amino acids with a complementation optimum at protein int ake of 5 g/kg BM/day where N-IRD was maximum. When feeding rats soy pr otein N-IRD(= 6.2 parts per thousand) did not increase, but declined s lightly above requirement intake of 10 g/kg BM/day to N-IRD = 5.7 part s per thousand at 30 g/kg BM/day. This indicates that the amino acid p attern of the metabolic pool was not complemented by intake of soy pro tein. These findings strongly suggest that the (endogenous) amino acid pattern of the metabolic pool, as present at zero protein intake, is characterized by an imbalance (''endogenous inbalance'') which may be complemented dependent on the intake of appropriate protein.