CARNITINE AFFECTS OCTANOATE OXIDATION TO CARBON-DIOXIDE AND DICARBOXYLIC-ACIDS IN COLOSTRUM-DEPRIVED PIGLETS - IN-VIVO ANALYSIS OF MECHANISMS INVOLVED BASED ON COA-ESTER AND CARNITINE-ESTER PROFILES

Newborn, colostrum-deprived piglets (n = 21) were used to study the ef fects of L-carnitine supplementation on the in vivo oxidation of [1-C- 14]octanoate to CO2 and dicarboxylic acids. Pigs were fitted with arte rial and bladder catheters and were infused with octanoate (supplying 35-100% of piglets' energy expenditure) and with or without valproate for a period of 24 h. After achieving steady-state octanoate oxidation , carnitine was coinfused [50 mu mol/kg(0.75) prime plus 20 mu mol/(h. kg(0.75))], and deviations in the octanoate oxidation rate, dicarboxyl ic acid excretion rate, and carnitine metabolism were monitored. At th e end of the 24-h infusion, samples of liver and muscle were analyzed for carnitine- and CoA-esters by HPLC. Carnitine stimulated octanoate oxidation by 7% (P < 0.05) and decreased dicarboxylic acid excretion b y 45% (P < 0.05). Carnitine supplementation increased (P < 0.05) conce ntrations of carnitine and acetyl carnitine in hepatic tissue (three- and 55-fold, respectively) and plasma (seven- and 11-fold); whereas, m uscle-carnitine concentration doubled upon carnitine supplementation, but acetyl carnitine concentration remained unaltered. Urinary excreti on of acetyl and free carnitine also increased with carnitine suppleme ntation, but accounted for <10% of carnitine infused. Hepatic total Co A and CoA esters increased with carnitine supplementation, whereas mus cle acetyl-CoA decreased. Valproate had only marginal effects on octan oate metabolism. These data confirm the hypothesis that carnitine affe cts the in vivo oxidation of octanoate in colostrum-deprived piglets a nd suggest that the effects may be mediated by aiding the export of ex cess acetyl groups from muscle or by enhancing uptake of octanoate int o liver mitochondria.