Showing papers on "Acyl-CoA published in 1974"

Cholesteryl ester synthesis in normal and atherosclerotic aortas of rabbits and rhesus monkeys

Abstract: The formation of cholesteryl ester in aortic tissue was studied using subcellular fractions from normal and atherosclerotic rabbit and rhesus monkey aortas. The properties of two enzyme systems capable of esterifying 1-14C-oleic acid into cholesteryl ester in vitro were investigated, and increased activity was demonstrated for both systems as a result of cholesterol feeding. Microsomal preparations were used to study the ATP, CoA-dependent esterification which involves two enzymes, fatty acyl CoA synthetase and fatty acyl CoA: cholesterol acyltransferase. The properties of both enzymes were investigated, and an increase of about fourfold in activity of the acryltransfrease was demonstrated in aortic microsomes as a result of cholesterol feeding for 3-6 months. Esterification of oleic acid into cholesteryl ester by aortic high-speed supernatant fractions at an acidic pH was also observed; the enzyme system involved did not require cofactors, and its activity greatly increased as a result of cholesterol fee...

Effect of 1,3-butanediol on hepatic fatty acid synthesis and metabolite levels in the rat.

Abstract: The effect of 1,3-butanediol on hepatic fatty acid synthesis and metab olite levels in the rat was examined. Hepatic fatty acid synthesis was depressed in rats fed 1,3-butanediol. An intraperitoneal injection of 1,3-butanediol increased blood glucose levels but did not affect hepatic fatty acid synthesis in the rat. Addition of 1,3-bu tanediol to the incubation buffer depressed glucose, but not acetate, conversion to fatty acids by rat liver slices. MA©thylA¨ne blue inhibition of hepatic fatty acid synthesis was partially reversed by the addition of 1,3-butanediol to the incubation buffer. Hepatic /3-hydroxybutyrate levels and the £-hydroxybutyrate:acetoacetate ratio were increased when 1,3-butanediol was fed. Lactate and pyruvate levels were lower in freeze-clamped liver preparations from rats fed 1,3-butanediol than those observed in control animals. Further, the lactate: pyruvate ratio was increased, suggesting that the hepatic cyto- plasmic NADH/NAD+ ratio was increased. Hepatic long-chain acyl CoA levels were also increased when 1,3-butanediol was fed. It is suggested that the shift in the cyto- plasmic redox state and the increase in hepatic long-chain acyl CoA levels are involved in the decrease in hepatic fatty acid synthesis observed when rats are fed 1,3-butanediol. J. Nutr. 104: 143&-1445, 1974.

Possibility of inborn defect in isovalericacidaemia involving altered enzyme specificity rather than total inactivity.

Abstract: TANAKA, Isselbacher and colleagues1 have described an inherited metabolic defect, isovalericacidaemia, which, though not fatal in their patients, leads, if untreated, to mental retardation and episodes of convlusion. As the name implies, the condition is characterised by high levels of isovaleric acid in the plasma. During periods of remission, this compound, which arises from the breakdown of dietary leucine, is excreted as a glycine conjugate. From the fact that only isovaleric acid accumulates and not butyric acid (from fat oxidation) or isobutyric or α-methyl butyric acids (from valine and isoleucine breakdown) Tanaka et al.1 have concluded that there must be a specific isovaleryl CoA dehydrogenase that is non-functional in isovalericacidaemia. It had been assumed previously2 that straight and branched-chain fatty acyl CoA compounds alike were oxidised by the green (that is, short-chain) acyl CoA dehydrogenase (see Fig. 1).