The cerebral metabolism of amino acids (AA) and ammonia in the postabsorptive state was evaluated in 8 subjects with normal renal function and in 6 patients with chronic renal insufficiency (CRI) by measuring the differences between the arterial and the internal jugular venous concentrations of free AA and ammonia. In normal conditions, the brain extracts serine, glutamine, proline, glycine, valine, 1/2 cystine, isoleucine, leucine, and lysine. In CRI, cerebral glycine and 1/2 cystine uptake increases, valine and isoleucine extraction decreases, glutamine uptake disappears, and ammonia extraction becomes evident. The cerebral extraction of glycine is correlated with the arterial concentration of glycine, serine, and branched-chain AA. The extraction of 1/2 cystine is correlated with the arterial concentration of 1/2 cystine and tyrosine. Finally, the extractions of valine and ammonia are correlated with the arterial concentration of valine and ammonia, respectively. It follows that alterations of blood AA and ammonia concentrations observed in CRI markedly affect the cerebral uptake of some AA and ammonia. The lack of cerebral glutamine extraction might be due to an enhanced production and/or, more likely, to an impaired utilization of this AA by the brain. Data reported here suggest that in CRI cerebral nitrogen metabolism is altered; such alterations may play a pathogenic role in uremic encephalopathy.
|Number of pages||6|
|Publication status||Published - 1981|
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