Attenuation of alcohol-induced hepatic fibrosis by polyunsaturated lecithin

Authors

  • Charles S. Lieber M.D.,

    Corresponding author
    1. Section of Liver Disease and Nutrition, Alcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center and Mount Sinai School of Medicine (CUNY), New York, New York
    • (151/G), Alcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center, Bronx, NY 10468
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  • Leonore M. Decarli,

    1. Section of Liver Disease and Nutrition, Alcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center and Mount Sinai School of Medicine (CUNY), New York, New York
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  • Ki M. Mak,

    1. Section of Liver Disease and Nutrition, Alcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center and Mount Sinai School of Medicine (CUNY), New York, New York
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  • Cho-Il Kim,

    1. Section of Liver Disease and Nutrition, Alcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center and Mount Sinai School of Medicine (CUNY), New York, New York
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  • Maria A. Leo

    1. Section of Liver Disease and Nutrition, Alcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center and Mount Sinai School of Medicine (CUNY), New York, New York
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  • Presented in part at the International Symposium on Phospholipids held December 4, 1989, in Cologne, FRG.

Abstract

Characteristic features of alcoholic liver injury include fibrosis and striking membrane alterations, with associated phospholipid changes. To offset some of these abnormalities, a 10-yr study was conducted in baboons: 12 animals (eight females, four males) were fed a liquid diet supplemented with polyunsaturated lecithin (4.1 mg/kcal) for up to 8 yr, with either ethanol (50% of total energy) or isocaloric carbohydrate. They were compared with another group of 18 baboons fed an equivalent amount of the same diet (with or without ethanol), but devoid of lecithin. In the two groups, comparable increases in lipids developed in the ethanol-fed animals, but striking differences in the degree of fibrosis were seen. Whereas at least septal fibrosis (with cirrhosis in two) and transformation of their lipocytes into transitional cells developed in seven of the nine baboons fed the regular diet with ethanol, septal fibrosis did not develop in any animals fed lecithin (p < 0.005). They did not progress beyond the stage of perivenular fibrosis (sometimes associated with pericellular and perisinusoidal fibrosis) and had a significantly lesser activation of lipocytes to transitional cells. Furthermore, when three of these animals were taken off lecithin, but continued on the same amount of the ethanol-containing diet, they rapidly (within 18 to 21 mo) progressed to cirrhosis, accompanied by an increased transformation of their lipocytes to transitional cells. These results indicate that some component of lecithin exerts a protective action against the fibrogenic effects of ethanol. Because we had previously found that choline, in amounts present in lecithin, has no comparable action, the polyunsaturated phospholipids themselves might be responsible for the protective effect. (HEPATOLOGY 1990;12:1390–1398).

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