Radioactive Fatty Acids Research Articles

Effects of aliphatic alcohols and fatty acids on the metabolism of acetate by rat liver slices.

The effects of the addition of normal aliphatic alcohols and fatty acids on the metabolism of acetate by rat liver slices have been investigated, with particular reference to the formation, from acetate-1-C14, of C14O2and radioactive lipids, proteins, and fatty acids. Whereas the addition of unlabelled acetate causes a fall in the rate of formation of C14O2, the decrease, at low concentrations, is less than that calculated for isotopic dilution. This is probably due to the fact that with an increased concentration of acetate there is an increased rate of acetate oxidation. However, the addition of ethanol causes a larger fall in the rate of formation of C14O2than would be expected if the alcohol were converted to acetate. This points to some inhibition by ethanol of acetate oxidation, a conclusion borne out by the inhibitory effects of n-alcohols on total CO2formation (in the absence and in the presence of added acetate) by rat liver slices. The fact, however, that the inhibitory effect of ethanol reaches a maximum at 5 mmolar and is constant to 50 mmolar points against a major inhibition due to ethanol per se. The results would be consistent with the conclusion that ethanol, at low concentrations, is more quickly converted into acetyl-CoA than acetate itself and that its speed of conversion into acetyl-CoA reaches a maximum at about 5 mmolar with rat liver slices. n-Propanol is much more inhibitory than ethanol but its effect is quantitatively identical with that of an equivalent quantity of propionate. Propionate and n-propanol are presumably rapidly converted to propionyl-CoA (or methyl malonyl-CoA), which is the effective inhibitor of acetate oxidation by its competition with acetyl-CoA. Propanol also shows direct inhibitory effects on acetate oxidation in rat liver slices. n-Butanol, n-pentanol, and n-hexanol have inhibitory effects identical with those of equivalent concentrations of corresponding fatty acids. These facts point to the oxidation, in rat liver, of aliphatic alcohols and fatty acids to propionyl-CoA or acetyl-CoA which inhibit C14O2formation from acetate-1-C14by competition or isotopic dilution. Alternations of inhibition occur between the odd- and even-numbered carbon alcohols and fatty acids which may be explained by the formation of mixtures of acetyl-CoA and the highly inhibitory propionyl-CoA from the long-chain alcohols and acids. Tribromoethanol is less inhibitory than propanol at equivalent concentrations though it is an effective inhibitor of acetate oxidation. Allyl alcohol is a much more potent inhibitor. Ethanol inhibits incorporation of radioactivity of acetate-1-C14into fatty acids in rat liver, the inhibition being approximately equal to, or possibly less than, that due to an equivalent quantity of acetate. This may be explained on the basis of isotopic dilution, by acetyl-CoA derived from the alcohol, with radioactive acetyl-CoA undergoing synthesis to radioactive fatty acids. Thus ethanol, at the concentrations investigated, by taking part in fatty acid synthesis, inhibits acetate conversion to fatty acids. Glucose shows the largest effect in stimulating fatty acid synthesis in the liver from acetate, fructose is less effective, and sorbitol shows no effect. The aliphatic alcohols inhibit incorporation of radioactivity from acetate-1-C14into liver lipids and proteins, propanol and pentanol showing the largest effects. There is an alternation between odd- and even-numbered aliphatic chains. The disappearance, or utilization, of acetate by rat liver slices is inhibited by the aliphatic alcohols, alternations between the odd- and even-numbered chains again being observable. The results are explained as being partly due to isotopic dilution and competition by acetyl-CoA and propionyl-CoA, and partly due to suppressions of acetate metabolism by the alcohols.

Further studies on the enzymic pattern of a cultured cell line from liver

The effect of insulin on the free fatty acid metabolism of Chang liver cells was observed to vary, depending on the growth rates of the cells. When the cells were not actively growing, insulin modestly increased the total recovery of radioactive fatty acid in lipid and produced a major increment of fatty acid in cellular triglyceride. During logarithmic growth of the cells these insulin changes were much less pronounced.

Effect of aureomycin on hepatic utilization of labeled body fat in rats.

SummaryAdministration of 5 mg Aureomycin to rats, the body fat of which had been labeled previously with C14-tripalmitin did not result in accumulation of excessive C14 activity in hepatic fatty acids. The amount and radioactivity of total fatty acids of carcass and of intestine were likewise similar in experimental and control animals. These findings are discussed in relation to the observation that Aureomycin causes an increase in incorporation of C14-acetate into hepatic fatty acids of rats. A 4-day metabolic balance study showed that from 81 to 93% of the fed tripalmitin was absorbed.

SYNTHESIS OF RADIOACTIVE FATTY ACIDS IN VITRO AND ITS HORMONAL CONTROL

SYNTHESIS OF RADIOACTIVE FATTY ACIDS IN VITRO AND ITS HORMONAL CONTROL

Hormonal influence upon the in vitro synthesis of radioactive fatty acids.

Hormonal influence upon the in vitro synthesis of radioactive fatty acids.

INHIBITION STUDIES ON RADIOACTIVE FATTY ACID METABOLISM

INHIBITION STUDIES ON RADIOACTIVE FATTY ACID METABOLISM

The Fate of C14-Labeled Palmitic Acid Administered Intravenously as a Tripalmitin Emulsion.

Summary1. In order to test the extent of utilization of fat emulsions in parenteral feeding, palmitic acid labeled with C14 at its sixth carbon was injected intravenously, in the form of the triglyceride, into fasted rats.2. From 36 to 59% of the administered C14 was expired as CO2 in 24 hours.3. Considerable amounts of the administered fatty acids were stored in adipose tissues throughout the body.4. The availability of intravenously administered tripalmitin for metabolic purposes is further shown by the finding that as much as 78% of the radioactive fatty acids recovered from the liver and small intestine had been incorporated into phospholipids.