Moderate Carnitine Depletion and Long-Chain Fatty Acid Oxidation, Exercise Capacity, and Nitrogen Balance in the Rat (original) (raw)

Carnitine plays a central role in lipid metabolism by transporting long-chain fatty acids into the mitochondria for @-oxidation. Reduction of carnitinc concentration docs not automatically imply that functional carnitine deficiency exists with direct consequences on energy metabolism. In our experimental model, we reduced tissue concentrations of carnitine to levels that arc comparable to those in patients with various metabolic disorders with secondary carnitine deficiency and did a study on the in vivo effects of moderate carnitine depletion on palmitate oxidation, excrcise capacity, and nitrogen balance. Thirty rats were divided into a carnitine-depleted group (group I) and pair-fed controls (group 11). Carnitine depletion resulting in a 48% reduction of tissue carnitine concentrations was induced by feeding ad libitum a carnitine-free oral diet consisting of parenteral nutrition solutions. Palmitate oxidation was measurcd by collecting cxpircd "CO, after an intrapcritoncal injection of [l-'JC]palmitatc, and exercise capacity was dctcrmined by having thc rats swim to exhaustion. Despite thc 48% dcplction of carnitinc in serum, muscle, and liver, there wcrc no diffcrcnccs in cumulative palmitate oxidation in 3 h (group I, 40 5 7%; group 11, 37 5 9% of injected activity), swimming time to exhaustion (group I, 8.1 5 2.8 h; group 11, 7.7 + 3.6 h), or nitrogen balance (group I, 1.1 r 0.5 g of nitrogenlkgld; group 11, 1.2 +-0.5 g of nitrogcnkgld). We concludc that carnitinc depiction of 48% has no effect on palmitatc oxidation, exercise capacity, or nitrogen balance in the rats studied. (Pedintr Res 36: [288][289][290][291][292] 1994)