The effects on lipid metabolism of long-term feeding of large amounts of ethanol or glucose differed from those that have been reported in short-term experiments. Three groups of male rats were investigated. The first was fed lab chow and 15% (v/v) ethanol ad lib.; the second was pair-fed with the first and given isocaloric amounts of glucose in lieu of ethanol; the third was fed lab chow and water ad lib. All three groups consumed nearly the same number of calories, and about 30% of the calories in the first group were derived from ethanol. Neither glucose nor ethanol added to a nutritionally adequate diet promoted the development of a fatty liver, although both stimulated acetate-(14)C utilization for hepatic lipid synthesis. In all three groups more than 80% of the label in hepatic lipid was found in fatty acids, and the distribution of label amongst the fatty acids of different chain lengths was virtually the same. Ethanol decreased while glucose increased the quantity of lipid in fat depots, and each altered the fatty acid composition of the lipids in adipose tissue, kidney, liver, and hepatic subcellular fractions in a different manner. The most striking of these changes was the relative increase in monounsaturated fatty acids and the decrease in essential fatty acids produced by glucose.

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PubMed1966

Effects of prolonged ingestion of glucose or ethanol on fatty acid synthesis by mitochondria and cell sap of rat liver and adipose tissue.

Effects of prolonged ingestion of glucose and ethanol on the rate of fatty acid synthesis by liver and adipose tissue have been investigated in male rats. Ethanol significantly enhanced the rate of fatty acid synthesis from malonyl-2-(14)C CoA in liver cell sap; glucose feeding enhanced the rate of fatty acid synthesis from both malonyl-2-(14)C and acetyl-1-(14)C CoA. Neither dietary supplement modified the types of fatty acid synthesized in this enzyme system. Palmitic acid was the principal product synthesized from a mixture of malonyl and acetyl CoA, whereas myristic and palmitic acids were the predominant products formed from acetyl CoA alone. Neither glucose nor ethanol affected fatty acid synthesis by adipose tissue cell sap. Mitochondria derived from liver and adipose tissue of control, glucose-fed, and ethanol-fed animals all incorporated acetyl-1-(14)C CoA into lipid at about the same rate, but did not utilize malonyl CoA for lipid synthesis to any significant degree. The label appeared in fatty acids, one-half of which were contained in phospholipid. Both unsaturated and saturated fatty acids synthesized by mitochondria contained isotope, most of which was present in the carboxyl groups. Ethanol and glucose feeding stimulated the labeling of monoenoic fatty acids in liver mitochondria, but only glucose did so for adipose tissue. These findings agree with results previously obtained when lipogenesis was measured with acetate-(14)C in vivo.

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