The lipid-lowering effect of carnitine and its precursors, namely lysine plus methionine, was examined in male Sprague-Dawley rats fed ethanol as 36% of the total calories. Ethanol caused typical hepatic steatosis characterized by significant accumulation of total lipids, triglycerides, cholesterols, phospholipids, and free fatty acids. Supplementation of the ethanol diet with 1% DL-carnitine, 0.5% L-lysine, and 0.2% L-methionine significantly lowered ethanol-induced increases of various lipid fractions, with the exception of free fatty acids. The lipid-lowering effect of carnitine was superior to that of its precursors and their effect together was no greater than that of carnitine alone. The triglyceride contents of liver and plasma were related inversely to the levels of carnitine and acyl carnitines. It is concluded that dietary carnitine more effectively than its precursors prevented alcohol-induced hyperlipemia and accumulation of fat in livers. Thus, a deficiency of functional carnitine may indeed exist in chronic alcoholic cases.

Distribution of carnitine and acylcarnitine in lumen flush and tissue of the small intestine was examined in four groups of male Sprague-Dawley rats fed either a nonpurified diet (groups 1, 2) or the same supplemented with 1% DL-carnitine (groups 3, 4). One group of animals under each dietary regimen (groups 2, 4) was fasted for 24 h prior to killing. Carnitine and acylcarnitines were present in higher concentrations in tissue of the small intestine than in the lumen flush. Even though the diets contained only traces of acid-soluble acylcarnitine, it was present in high concentrations both in tissue of the small intestine and lumen flush. Proximal segments of small intestine tended to concentrate carnitine and acylcarnitines under all conditions of treatment. Carnitine supplementation increased the amounts of carnitines in tissue; however, there was only a minor alteration in the pattern of distribution of carnitine and acylcarnitines.