Amino acid profiles and muscle protein composition in rats with a reduced renal mass in the fed state.
In severe chronic renal failure (CRF) with associated metabolic acidosis, abnormalities in protein metabolism and amino acid (AA) profiles in the fed state are well described. To evaluate the effect of early uraemia and the influence of acid-base status on protein metabolism and AA profiles, three groups of pair-fed rats were studied: group I - rats with 1+ 1/2 nephrectomy; group II - rats with 1+ 1/2 nephrectomy receiving NaHCO3 supplementation, and group III - sham-operated rats with NaHCO3 supplementation. After 4 weeks, serum creatinine values were similar in groups I and II (111 +/- 5 and 119 +/- 4 mumol/l) and higher than in group III (51 +/- 5 mumol/l, p < 0.0001); HCO-3 was reduced only 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 increased levels of phenylalanine, glycine, glutamate, proline and alanine. The marked increase of threonine in group I was corrected by NaHCO3 supplementation in group II. The total nonessential AA were higher both in group I (1,832 +/- 53 mumol/l, p < 0.05) and group II (1,788 +/- 103 mumol/l, p < 0.05) than in group III (1,542 +/- 54 mumol/l). These results are similar to those described in the fed state of uraemic patients. Intracellular AA changes were detected, especially in group 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 results show that AA abnormalities in the fed state occur early in the course of CRF, and that the marked increase of threonine is corrected by NaHCO3 supplementation. These data suggest that either an impaired utilization of the ingested proteins might occur before the appearance of major alterations in endogenous protein metabolism or acid-base status might alter AA metabolic rate per se.
Cupisti
A
A
Department of Nephrology, Leicester General Hospital, UK.
Baker
F
F
Bevington
A
A
Brown
J
J
Lock
C
C
Harris
K P
KP
Walls
J
J
D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000097:blood; D000596:Amino Acids / Q000032:analysis / Q000097:blood*; D000818:Animals; D001639:Bicarbonates / Q000097:blood; D001835:Body Weight; D003404:Creatinine / Q000097:blood; D004435:Eating; D005260:Female; D007668:Kidney / Q000737:chemistry / Q000473:pathology* / Q000601:surgery; D007676:Kidney Failure, Chronic / Q000097:blood / Q000473:pathology; D009124:Muscle Proteins / Q000032:analysis*; D018482:Muscle, Skeletal / Q000737:chemistry; D009392:Nephrectomy; D011506:Proteins / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014511:Uremia / Q000097:blood
D000596:Amino Acids; D001639:Bicarbonates; D009124:Muscle Proteins; D011506:Proteins; D003404:Creatinine