A. Cupisti et al., AMINO-ACID PROFILES AND MUSCLE PROTEIN-COMPOSITION IN RATS WITH A REDUCED RENAL MASS IN THE FED STATE, Nephron, 74(1), 1996, pp. 183-188
In severe chronic renal failure (CRF) with associated metabolic acidos
is, abnormalities in protein metabolism and amino acid (AA) profiles i
n the fed state are well described. To evaluate the effect of early ur
aemia and the influence of acid-base status on protein metabolism and
AA profiles, three groups of pair-fed rats were studied: group I - rat
s with 1+1/2 nephrectomy; group II - rats with 1+1/2 nephrectomy recei
ving NaHCO3 supplementation, and group III - sham-operated rats with N
aHCO3 supplementation. After 4 weeks, serum creatinine values were sim
ilar in groups I and II (111 +/- 5 and 119 +/- 4 mu mol/l) and higher
than in group III (51 +/- 5 mu mol/l, p < 0.001); HCO3- was reduced on
ly in group I (22.4 +/- 0.8 mmol/l) compared to group II (28.3 +/- 0.6
mmol/l, p < 0.001) and group III (28.2 +/- 1.3 mmol/l, p < 0.001). In
the uraemic animals (groups I and II) arterial AA profiles showed inc
reased levels of phenylalanine, glycine, glutamate, proline and alanin
e. The marked increase of threonine in group I was corrected by NaHCO3
supplementation in group II. The total nonessential AA were higher bo
th in group I (1,832 +/- 53 mu mol/l, p < 0.05) and group II (1,788 +/
- 103 mu mol/l, p < 0.05) than in group III (1,542 +/- 54 mu mol/l). T
hese results are similar to those described in the fed state of uraemi
c patients. Intracellular AA changes were detected, especially in grou
p II, namely increased glycine and a decrease in threonine and serine
levels. No signs of malnutrition or changes in alkali-soluble protein
(ASP) or ASP/DNA ratio in liver and muscle were observed. These result
s show that AA abnormalities in the fed state occur early in the cours
e of CRF, and that the marked increase of threonine is corrected by Na
HCO3 supplementation. These data suggest that either an impaired utili
zation of the ingested proteins might occur before the appearance of m
ajor alterations in endogenous protein metabolism or acid-base status
might alter AA metabolic rate per se.