Hepatic Synthesis of Apoproteins of Very Low Density and High Density Lipoproteins in Perfused Rat Liver: Influence of Chronic Heavy and Moderate Doses of Ethanol

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Abstract
The effects of 6 weeks of heavy and moderate ethanol feeding to rats upon lupids and lipoprotein metabolism were determined. As compared to thecontrol group, the heavy ethanol feeding resulted in the following changes: liver weight/kilogram body weight increased by 48% (p < 0.001) with a concomitant 52% increase (p < 0.001) in liver protein/kilogram body weight and a 2.75-fold (p < 0.001) increase in liver total lipids/kilogram body weight. In contrast, liver DNA/kilogram body weight or per liver was not affected significantly. Plamsa cholesterol and triglycerides were higher by 53% (p < 0.01) and 77% (p < 0.01), respectively. Liver cholesterol and triglycerides were 4.4-fold and 3.8-fold higher (p < 0.001), respectively. Plasma total A1 was 1.72-fold higher (p < 0.001), whereas there was no significant difference in plasma apo E levels between the two groups. However, plasma high density lipoproteins (HDI) apo E was 48% lower (p < 0.02) while the very low density lipoproteins (VLDL)E was 2.15-fold higher (p < 0.02). Hepatic totalprotein synthetic rate in the ethanol group was not significantly different from the control group. In contrast, labeled leucine incorporation into the total secretory proteins was inhibited by 36% (p < 0.01) in ethanol-fed group. Specifically, inhibitions of the synthetic rates of various secretory proteins in the ethanol group compared to the control group were as follows: by 55% (p < 0.005) for total VLDL aproproteins, by 44% (p < 0.05) for apo A1 protein, by 55% (p < 0.001) for total ape E proteins, by 62% (p < 0.001) for VLDL apo E, by 52% (p < 0.001) for HDL apo E and by 50% (p < 0.001) for transferrin. In contrast, moderate ethanol feeding for six weeks did not alter any of the above parameters. Thus, impaired synthesis/secretion of VLDL and HDL could be the major cause for fatty liver after alcohol abuse.