Carnitine ester hydrolysis in arteries from normal and cholesterol-fed rabbits and the effects of carnitine esters on arterial microsomal ACAT.
Carnitine ester hydrolysis was observed in homogenates of normal rabbit (Oryctolagus cuniculus) aortas and in intact aortas from normal and cholesterol-fed rabbits using [14C]palmitoylcarnitine as a substrate. Hydrolytic activity was decreased approximately 50% in arterial tissue from cholesterol-fed rabbits and may account for the observation that carnitine esters accumulate in arteries of animals fed atherogenic diets. Long-chain acylcarnitines (C14-C18) were found to be moderate inhibitors of microsomal acylCoA:cholesterol acyltransferase (ACAT, EC 2.3.1.26); short-chain acylcarnitine (C2-C10) and carnitine itself were not inhibitors. The data suggest that the increase in activity of arterial ACAT that characteristically parallels the development of atherosclerosis does not occur as a result of carnitine ester accumulation.
D000818:Animals; D001013:Aorta, Thoracic / Q000201:enzymology / Q000378:metabolism*; D002331:Carnitine / Q000031:analogs & derivatives* / Q000494:pharmacology; D002791:Cholesterol, Dietary / Q000494:pharmacology*; D006868:Hydrolysis; D007700:Kinetics; D008297:Male; D008861:Microsomes / Q000201:enzymology*; D010172:Palmitoylcarnitine / Q000378:metabolism*; D011817:Rabbits; D002785:Sterol O-Acyltransferase / Q000378:metabolism*
D002791:Cholesterol, Dietary; D010172:Palmitoylcarnitine; D002785:Sterol O-Acyltransferase; D002331:Carnitine