Metabolic effects of L-phenyllactate in perfused kidney, liver, and muscle

L-Phenyllactate (L-PL) can promote growth of normal and germ-free rats eating a phenylalanine (Phe)-free diet, but the sites and pathway of its conversion to Phe have not been extensively studied. We perfused rat kidneys, livers, and hindquarters with L-PL and measured Phe release and effects on organ function. Renal release of Phe the during perfusion with L-PL was 3.0 times control (P less than 0.001) and increased 2.5-fold with addition of glutamine (P less than 0.001); with phenylpyruvate (PP), it was 3.5 times control (P less than 0.001). Sixty-four percent of L-PL disappearance could be accounted for by appearance of PP and Phe. Although renal gluconeogenesis from lactate was inhibited 28% by L-PL, neither glomerular filtration rate (0.44 ml . min-1 . g wet weight-1) nor sodium reabsorption (94.3%) were impaired. There was no net release of Phe or PP by rat livers or hindquarters perfused with L-PL and hepatic gluconeogenesis, urea synthesis, and potassium balance were unaffecte by L-PL. Thus, the kidney, but not skeletal muscle or liver, converts L-PL to Phe, presumably by the pathway L-PL leads to PP leads to Phe. In acute experiments with isolated organs, L-PL does not cause significant renal or hepatic dysfunction.