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Research Article Free access | 10.1172/JCI116981
Division of Clinical Nutrition and Metabolism, School of Medicine, University of California, Davis 95616.
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Division of Clinical Nutrition and Metabolism, School of Medicine, University of California, Davis 95616.
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Division of Clinical Nutrition and Metabolism, School of Medicine, University of California, Davis 95616.
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Division of Clinical Nutrition and Metabolism, School of Medicine, University of California, Davis 95616.
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Division of Clinical Nutrition and Metabolism, School of Medicine, University of California, Davis 95616.
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Published January 1, 1994 - More info
This study investigated the mechanism by which chronic ethanol feeding reduces arachidonate and other highly unsaturated fatty acids in pig liver phospholipids. Five micropigs were fed a diet providing 89 kcal/kg body wt for 12 mo, with ethanol and fat as 40 and 34% of energy, respectively. Five control pigs were pairfed corn starch instead of ethanol. The activities of delta 6 and delta 5 desaturases (expressed as microsomal conversion of precursor to product) in liver from ethanol-fed pigs were reduced to less than half that of controls, whereas the activity of delta 9 desaturase was unaffected in the ethanol group. delta 5 Desaturase activity showed positive correlation with the abundance of its products in liver total phospholipids and microsomes in the ethanol group, but not in the controls. Correlation between delta 6 desaturase activity and its products showed similar pattern to that of delta 5 desaturase, but did not reach statistical significance. No difference was observed between the two groups in coenzyme A concentration in the liver. These results suggest that the selective reduction of delta 6 and delta 5 desaturase activities, not the microsomal electron transport system, are directly responsible for the altered profile of liver phospholipids.