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  • Journal
    Digital Access PubMed Central v. 1-, 1928-
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    v. 1-79, 1928/29-2006.
    75
  • Article
    Arakawa M, Taketomi S, Furuno K, Matsuo T, Iwatsuka H.
    J Nutr. 1975 Dec;105(12):1500-8.
    Mechanisms involved in the development of the alcoholic fatty liver in KK-Ay mice were investigated. Incorporation studies using [14C]acetate and [3H]palmitate indicated that the half-life of hepatic triglycerides was doubled in the ethanol-ingesting mice, and utilization of the exogenous fat was significantly increases as compared with that of the control. No persistent alteration was recognized in hepatic oxidation of palmitate, as estimated by in vitro experiments using liver slices obtained from control and ethanol-drinking mice. Enzymic studies indicated that the activities of acetyl COA carboxylase, ATP citrate lyase, malic enzyme, and 6-phosphogluconate dehydrogenase were increased with ethanol drinking. The increment in hepatic triglycerides accumulated during ethanol ingestion was largely accounted for by palmitoleic, oleic, and linoleic acids. These findings demonstrated an augmentation in hepatic lipogenesis as well as an increased utilization of exogenous fats. Ethanol drinking did not cause any appreciable change in plasma triglyceride level and metabolism of adipose tissue. In summary of the present studies, accelerated lipogenesis and increased utilization of the dietary fats may be possible causal factors in the alcoholic fatty liver of KK-Ay mice.
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