Moderate carnitine depletion and long-chain fatty acid oxidation, exercise capacity, and nitrogen balance in the rat.

Carnitine plays a central role in lipid metabolism by transporting long-chain fatty acids into the mitochondria for beta-oxidation. Reduction of carnitine concentration does 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 are 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, exercise capacity, and nitrogen balance. Thirty rats were divided into a carnitine-depleted group (group I) and pair-fed controls (group II). 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 measured by collecting expired 14CO2 after an intraperitoneal injection of [1-14C]palmitate, and exercise capacity was determined by having the rats swim to exhaustion. Despite the 48% depletion of carnitine in serum, muscle, and liver, there were no differences in cumulative palmitate oxidation in 3 h (group I, 40 +/- 7%; group II, 37 +/- 9% of injected activity), swimming time to exhaustion (group I, 8.1 +/- 2.8 h; group II, 7.7 +/- 3.6 h), or nitrogen balance (group I, 1.1 +/- 0.5 g of nitrogen/kg/d; group II, 1.2 +/- 0.5 g of nitrogen/kg/d). We conclude that carnitine depletion of 48% has no effect on palmitate oxidation, exercise capacity, or nitrogen balance in the rats studied.