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.