The metabolism of racemic sodium lactate in the presence of disease of the liver has been studied by Schumacher1 and Hartmann and Senn.2 The two optically active enantiomer components constituting racemic lactate differ from each other, according to Cori and Cori,3 with regard to the manner of their biologic utilization. The l form when injected or ingested cannot be converted into glycogen or any intermediate carbohydrate, but its greater portion reappears in the urine, whereas the remainder may be accounted for by the formation of accessory carbon dioxide. On the other hand, d-lactate is converted into glycogen by the liver.4 Hartmann and Senn concluded that the degree of glycogen formation from racemic lactate depends on the proportion of the d form present in the mixture.
It seems, therefore, of importance to study the fate of the optically active components separately, especially that of the d
SOFFER LJ, DANTES DA, NEWBURGER R, SOBOTKA H. METABOLISM OF SODIUM d-LACTATE: II. UTILIZATION OF INTRAVENOUSLY INJECTED SODIUM d-LACTATE BY PATIENTS WITH ACUTE DIFFUSE PARENCHYMAL INJURY OF THE LIVER. Arch Intern Med (Chic). 1937;60(5):882–886. doi:10.1001/archinte.1937.00180050149011
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