Role of omega oxidation of fatty acids in formation of the acetyl unit for acetylation.

Specifically W-labeled fatty acids and 2-amino-4-phenylbutyric acid were administered to fed and starved normal and nonketotic and ketotic diabetic rats. The acetylated amino acid was isolated from their urines, hydrolyzed, and the resulting acetates degraded. The percentage of distribution of 14C! in the acetate from [2-Wlstearate and [2W]palmitate formed by the nonketotic diabetic rats was about carbon 1 = 5% and carbon 2 = 95%. For terminally labeled laurate, palmitate, and stearate it was about carbon 1 = 30% and carbon 2 = 70%. Similar distributions were found in the acetates formed by the normal and ketotic diabetic rats, although incorporation into carbon 1 from [16Wlpalmitate was less. These distributions mean that a significant portion of the acetyl carbons arose by other than j3 oxidation of the fatty acids. The only presently known pathway by which greater incorporation of 14C into carbon 1 of the acetyl group can occur from an &C-fatty acid than a 2-W-labeled fatty acid is via w oxidation. The distributions allow the estimation that about 40% of the initial oxidation of the fatty acids from which the acetyl carbons are derived in the nonketotic diabetic rat is w oxidation and the remainder is /3 oxidation. The distribution of radioactivity in acetate formed from [lo‘Vlpalmitate was about carbon 1 = 15% and carbon 2 = 85%, suggesting that only a portion of the dicarboxylic acids formed via w oxidation is oxidized to completion via p oxidation in the environment where amino acid acetylation occurs.