The effect of excess (acyl) carnitine on lipid metabolism in rat heart.
During Langendorff perfusion of rat hearts with Intralipid, the resulting fat accumulation in the hearts can be inhibited by the addition of 5 mM L-carnitine to the perfusion medium. The mechanism of this phenomenon is probably the inhibition of lipid accumulation in the heart by acylcarnitine rather than stimulation of fatty acid oxidation by excess carnitine addition. Palmitoylcarnitine was found to stimulate trioleoylglycerol hydrolysis at neutral pH in heart homogenates, when it was tested in the presence of relatively much protein. At higher palmitoylcarnitine: protein ratios, however, lipolysis was inhibited. Inhibition of lipolysis was also observed in lipid-enriched hearts during retrograde perfusion by the addition of 5 mM carnitine suggesting that also in intact heart long-chain acylcarnitine excess may inhibit lipolytic activity.
D000818:Animals; D002331:Carnitine / Q000494:pharmacology*; D005217:Fat Emulsions, Intravenous / Q000378:metabolism*; D005227:Fatty Acids / Q000378:metabolism; D005992:Glycerol-3-Phosphate O-Acyltransferase / Q000037:antagonists & inhibitors; D006863:Hydrogen-Ion Concentration; D006868:Hydrolysis; D050356:Lipid Metabolism; D008071:Lipoprotein Lipase / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D010084:Oxidation-Reduction; D010172:Palmitoylcarnitine / Q000494:pharmacology; D051381:Rats; D014280:Triglycerides / Q000378:metabolism; D014304:Triolein / Q000378:metabolism
D005217:Fat Emulsions, Intravenous; D005227:Fatty Acids; D014280:Triglycerides; D014304:Triolein; D010172:Palmitoylcarnitine; D005992:Glycerol-3-Phosphate O-Acyltransferase; D008071:Lipoprotein Lipase; D002331:Carnitine