NO REPLENISHMENT OF CARNITINE FROM TRIMETHYLLYSINE DURING PIVALATE-INDUCED CARNITINE LOSS IN HUMANS

Pivaloylcarnitine formation from exogenous carnitine and from carnitin e precursor 6-N-trimethyllysine was investigated in two groups of piva mpicillin treated subjects. In this first group, medication of pivampi cillin led to the formation of and urinary excretion of pivaloylcarnit ine. Oral L-carnitine supplementation, introduced after the third day of treatment, caused 2 fold urinary excretion of carnitine esters. For this group, the plasma levels and urinary output of butyrobetaine als o decreased on the third day of pivampicillin treatment, but it normal ized after carnitine administration. In contrast, urinary output of th e carnitine precursor, trimethyllysine did not change during the study period. For the second group, oral trimethyllysine supplementation wa s started on the 4th day of pivampicillin treatment. Administration of trimethyllysine had no effect on the urinary output of carnitine este rs, although the urinary excretion of it increased from approximately 25 to 450 mu mol/day. Plasma levels and urinary output of butyrobetain e decreased during the pivampicillin treatment and administration of t rimethyllysine did not restore the levels. Administration of trimethyl lysine produced a large increase in urinary trimethyllysine output, bu t it did not affect the fast atom bombardment mass spectrometry signal intensity of other carnitine precursors. The urinary metabolite profi le shows, that the conversion process of trimethyllysine to hydroxy-tr imethyllysine represent an obstacle in the butyrobetaine and carnitine biosynthesis in humans in vivo. Because the administered trimethyllys ine was not converted to carnitine or carnitine precursors to any sign ificant extent, its nutritional value with respect to the replenishmen t of carnitine reserves is questionable. (C) Elsevier Science Inc. 199 7.