Abstract: Abnormalities of muscle protein stores in uremia result from changes in the components of protein turnover. In vivo measurements of protein synthesis and degradation in uremia are subject to several errors. There may be incomplete equilibration of the infused labeled amino acid with the precursor pool for protein synthesis because of abnormal amino acid transport into muscle and increased catabolism of the infused amino acid. The infusion technique for measuring protein degradation cannot differentiate between rates occurring in different tissues. Moreover, measurement of 3-methylhistidine as an estimate of muscle protein degradation is invalid in uremia because its renal clearance is impaired. In vitro studies using radiolabeled amino acids should give more reliable estimates of the components of muscle protein turnover. Estimation of the rate of protein synthesis with a labeled amino acid still requires measurements of its specific activity in the precursor pool for protein synthesis, but this can be accomplished more easily in vitro. The factors known to affect protein synthesis and degradation in normal muscle, which are most likely to affect protein turnover in uremic muscle, are insulin-resistance and maladaptation to fasting. Few studies of the components of protein turnover in uremia have examined the effect of these or other factors.
Publication Year: 1983
Publication Date: 1983-12-01
Language: en
Type: article
Indexed In: ['pubmed']
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Cited By Count: 32
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