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Difference in Hepatic Metabolism of Long- and Medium-Chain Fatty Acids: the Role of Fatty Acid Chain Length in the Production of the Alcoholic Fatty Liver*

Charles S. Lieber, André Lefèvre, Norton Spritz§, Lawrence Feinmanǁ and Leonore M. DeCarli

Liver Disease and Nutrition Unit, Second (Cornell) Medical Division, Bellevue Hospital, and the Department of Medicine, Cornell University Medical College, New York

Recipient of a U. S. Public Health Service Research Career Development Award (K3-AM-22,590) from the National Institute of Arthritis and Metabolic Diseases.

§ Established Investigator of the Health Research Council of the City of New York (I-128), Present address: The Rockefeller University, New York, N. Y.

ǁ Supported by a Postdoctoral Research Traineeship in Gastroenterology (TI AM 5091) and a Research Fellowship (F2 AM29096-01) from the National Institute of Arthritis and Metabolic Diseases, U. S. Public Health Service.

* Submitted for publication 20 March 1967; accepted 8 June 1967.

Published September 1967

Replacement of dietary triglycerides containing long-chain fatty acids (LCFA) by triglycerides containing medium-chain fatty acids (MCFA) markedly reduced the capacity of alcohol to produce fatty liver in rats. After 24 days of ethanol and MCFA, the increase in hepatic triglycerides was only 3 times that of controls, whereas an 8-fold rise was observed after ethanol and LCFA. The triglyceride fatty acids that accumulated in the liver after feeding of ethanol with MCFA contained only a small percentage of the MCFA; their composition also differed strikingly from that of adipose lipids.

To study the mechanism of the reduction in steatosis, we compared oxidation to CO2 and incorporation into esterified lipids of 14C-labeled chylomicrons or palmitate-14C (representing LCFA), and of octanoate-14C (as MCFA) in liver slices and isolated perfused livers, in the presence or absence of ethanol. Ethanol depressed the oxidation of all substrates to CO2; MCFA, however, was much more oxidized and reciprocally much less esterified than LCFA, with a 100-fold difference in the ratio of esterified lipid-14C to 14CO2. Furthermore, in hepatic microsomal fractions incubated with α-glycerophosphate, octanoate was much less esterified than palmitate. This propensity of MCFA to oxidation rather than esterification represents a likely explanation for the reduction in alcoholic steatosis upon replacement of dietary LCFA by MCFA.

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