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H Osmundsen

Publications and source records attributed to H Osmundsen.

At least 55 records · Page 3Linked to original sources
PubMed1982

Factors which can influence beta-oxidation by peroxisomes isolated from livers of clofibrate treated rats. Some properties of peroxisomal fractions isolated in a self-generated Percoll gradient by vertical rotor centrifugation.

1. Oxidation of radioactivity labeled acyl-CoA esters by apparently intact peroxisomes, isolated from rats treated with clofibrate, was stimulated by about 100% by added oxaloacetate. Added pyruvate gave much smaller stimulation. This stimulation is proposed to be due to re-oxidation of NADH generated during peroxisomal beta-oxidation of acyl-CoA esters. 2. Additions of these alpha-ketoacids, and of CoA, were found to influence extent of peroxisomal beta-oxidation of [U-14C]palmitoyl-CoA. Various concentrations of added CoA was markedly less inhibitory to oxidation of [14-14C]erucoyl-CoA and [10-14C]elaidoyl-CoA, as compared to [U-14C]palmitoyl-CoA. 3. Added NADP+, at concentrations higher than 0.5 mM, added NADPH and NADH were inhibitory to peroxisomal beta-oxidation of [U-14C]palmitoyl-CoA. Significant inhibition was found at concentrations which were too high for this to be of significance in vivo.

Animals↗
PubMed1982

Synthesis of unsaturated carnitine esters with N-acyl imidazoles.

A novel procedure is described for the synthesis of acylcarnitines. This entails the synthesis of an N-acyl imidazole intermediate, which subsequently is reacted with L-carnitine perchlorate to form the acylcarnitine. The procedure is rapid and simple, and does not require a large excess of N-acyl imidazole to achieve a reaction yield of 50-70%. A procedure, based on reverse-phase Sep-Pak cartridges for rapid isolation of acylcarnitines from these reaction mixtures is also described. These procedures have, in particular, been applied in the synthesis of polyunsaturated acylcarnitines, including docosahexaenoylcarnitine.

Acylation↗
PubMed1981

Effects of high-fat diets on hepatic fatty acid oxidation in the rat. Isolation of rat liver peroxisomes by vertical-rotor centrifugation by using a self-generated, iso-osmotic, Percoll gradient.

1. Rat liver peroxisomal fractions were isolated in iso-osmotic Percoll gradients by using vertical-rotor centrifugation. The fractions obtained with rats given various dietary treatments were characterized. 2. The effect on peroxisomal beta-oxidation of feeding 15% by wt. of dietary fat for 3 weeks was investigated. High-fat diets caused induction of peroxisomal beta-oxidation, but diets rich in very-long-chain mono-unsaturated fatty acids produced a more marked induction. 3. Peroxisomal beta-oxidation induced by diets rich in very-long-chain mono-unsaturated fatty acids can oxidize such acids. Trans-isomers of mono-unsaturated fatty acids are oxidized at rates that are faster than, or similar to, those obtained with corresponding cis-isomers. 4. Rates of oxidation of [14-14C]erucic acid by isolated rat hepatocytes isolated from rats fed on high-fat diets increased with the time on those diets in a fashion very similar to that previously reported for peroxisomal beta-oxidation [see Neat, Thomassen & Osmundsen (1980) Biochem, J. 186, 369-371]. 5. Total liver capacities for peroxisomal beta-oxidation (expressed as acetyl groups produced per min) were estimated to range from 10 to 30% of mitochondrial capacities, depending on dietary treatment and fatty acid substrate. A role is proposed for peroxisomal beta-oxidation in relation to the metabolism of fatty acids that are poorly oxidized by mitochondrial beta-oxidation, and, in general, as regards oxidation of fatty acids during periods of sustained high hepatic influx of fatty acids.

Animals↗
PubMed1981

Clofibrate.

Explore the source record for details and available documents.

Animals↗
PubMed1980

Induction of peroxisomal beta-oxidation in rat liver by high-fat diets.

Liver peroxisomes were prepared by using a Percoll gradient in a vertical rotor. beta-Oxidation was measured in peroxisomes isolated from livers of rats fed on either high-(15% by wt.) or low- (5% by wt.) fat diets. The feeding of high-fat diets gave a 1.4-2.4-fold increase in total liver peroxisomal beta-oxidation, and a similar increase in specific activity. A 1.5-4.5-fold increase was seen in the specific activity of purified peroxisomal preparations. The reasons for these increases are discussed.

Animals↗
PubMed1979

Associative properties of butyryl-coenzyme A synthetase from ox liver mitochondria.

Butyryl-coenzyme A synthetase (butyrate:CoA ligase (AMP-forming), EC 6.2.1.2) from an acetone-dried powder of ox liver mitochondria was found to have a molecular weight of approx. 40 000. The sedimentation equilibrium analysis suggested the presence in solution of higher molecular weight forms of the enzyme and these could also be obtained by extracting the enzyme from the mitochondrial powder in non-reducing conditions. The enzyme was inhibited by sulphydryl reagents, and was found to have at least one available thiol group/molecule. The relationship between enzymic activity and concentration was non-linear, and suggested that an inactive monomer-active dimer equilibrium was present. The 5--6-fold activation by bovine serum albumin required the presence of free thiol groups in the albumin and involved association of albumin with the enzyme.

Animals↗
PubMed1978

Comparative biochemistry of beta-oxidation. An investigation into the abilities of isolated heart mitochondria of various animal species to oxidize long-chain fatty acids, including the C22:1 monoenes.

Rates of acylcarnitine oxidation by isolated heart mitochondria from various animal species were measured polarographically, and by using a spectrophotometric assay [see Osmundsen & Bremer (1977) Biochem. J. 164, 621-633]. Polarographic measurements do not give a correct guide to abilities to beta-oxidize very-long-chain acylcarnitines, in particular C22:1 fatty acylcarnitines. 2. No significant species differences were detected in the abilities to beta-oxidize various C22:1 fatty acylcarnitines. Significant species differences were, however, detected when rates of beta-oxidation were correlated with rates of respiration brought about by very-long-chain acylcarnitines. We concluded that some aspects of oxidative metabolism (possibly the oxidation of tricarboxylic acid-cycle intermediates) are inhibited by very-long-chain fatty acids in some species (e.g. the rat and the cat but not in others (e.g. the pig and the rabbit). 3. It is proposed that the pattern of variation of rates of oxidation of various acylcarnitines (as measured spectrophotometrically) of various chain lengths can be used as a guide to the chain-length specificities of the acyl-CoA dehydrogenases of beta-oxidation (EC 1.3.99.3).

Animals↗
PubMed1978

The effects of hypoglycin on glucose metabolism in the rat. A kinetic study in vivo and [U-14C,2-3H]glucose.

1. The kinetics of glucose metabolism were evaluated in rats deprived of food 15-21 h after the administration of hypoglycaemic doses of hypoglycin (100 mg/kg body wt.) by following changes in the specific radioactivities of 14C and 3H in blood glucose after an intravenous dose of [U-14C,2-3H]glucose [Katz, Rostami & Dunn (1974) Biochem. J. 142, 161-170]. 2. During this time, recycling of glucose through the Cori cycle was virtually abolished, the rate of irreversible disposal of glucose and its total body mass were both decreased by about 70%, whereas there was little effect on the mean transit time for glucose. 3. It was concluded that hypoglycaemia is due to inhibition of gluconeogenesis.

Animals↗