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
Tatg. Vankempen et J. Odle, 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, The Journal of nutrition, 125(2), 1995, pp. 238-250
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.