AJP - Endocrinology and Metabolism, Vol 238, Issue 5 450-E457, Copyright © 1980 by American Physiological Society
Metabolic effects of L-phenyllactate in perfused kidney, liver, and muscle
V. U. Collier, D. O. Butler and W. E. Mitch
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.
