Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Caproates”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources
PubMed1978

Transient and long-term differential modulations of branched-chain alpha-keto acid decarboxylase activity in hypophysectomized rats.

Hypophysectomy caused a marked but transient increase in branched-chain alpha-keto acid decarboxylase activities in rat liver mitochondria, peaking at about nine days post-surgery. The magnitude of increase is different for each of the three branched-chain alpha-keto acids. The activities then fall to a new steady state in three weeks with alpha-ketoisovalerate decarboxylase activity within the normal range, alpha-keto-beta-methylvalerate decarboxylase activity at twice normal, and alpha-ketoisocaproate decarboxylase activity decreased to a level too low for accurate measurements.

Animals↗
PubMed1979

Studies on the role of beta-cell metabolism in the insulinotropic effect of alpha-ketoisocaproic acid.

alpha-Ketoisocaproic acid has been shown to be a potent insulin secretagogue but the mechanism has not been elucidated. To define the role of beta-cell metabolism in the insulinotropic activity of alpha-ketoisocaproic acid the utilization of glucose and the oxidation of alpha-ketoisocaproic and isovaleric acid by incubated islets of obese hyperglycemic mice were measured. Glucose metabolism was never enhanced by alpha-ketoisocaproic acid. The same 14CO2 amounts were released from the non-secretagogue [1-14C]isovaleric acid (10 mM) or from alpha-keto[2-14C]isocaproic acid (5--20 mM). Pyruvate (20 mM) did not inhibit alpha-ketoisocaproic acid-induced insulin secretion in spite of reduction of decarboxylation of alpha-ketoisocaproic acid by more than 40%. The results indicate that stimulated insulin release in response to alpha-ketoisocaproic acid is not mediated by an indirect increase in glucose metabolism and further suggest that isovaleryl-CoA and following CoA-esters in alpha-ketoisocaproic acid degradation are not likely recognized as signals. The possibility, however, remains that enhanced intramitochondrial production of reducing equivalents elicits insulin secretion.

Animals↗
PubMed1979

Effect of L-leucine on p-aminohippurate accumulation by mammalian renal cortical slices.

The effect of several amino acids (L-glutamate, L-phenylalanine, L-leucine, glycine, L-tryptophan, L-histidine, L-valine) on p-aminohippurate accumulation was evaluated in rat, mouse and rabbit kidneys. Only leucine was found to enhance p-aminohippurate accumulation in rat and mouse renal cortical slices but not in rabbit slices. Leucine had no effect on tetraethylammonium accumulation. In rat renal cortical slices, leucine increased the uptake and decreased the runout of p-aminohippurate, each effect contributing to the increase in p-aminohippurate accumulation. The apparent Km of p-aminohippurate uptake was decreased by leucine with no change in the apparent V. Aminooxyacetate (an inhibitor of transamination of leucine) partially depressed the stimulating effect of leucine on p-aminohippurate accumulation, whereas alpha-ketoisocaproic acid (a metabolite of leucine formed by transamination) enhanced p-aminohippurate accumulation, suggesting that the metabolism of leucine in kidney slices may be necessary for the stimulating effect on p-aminohippurate transport.

Amino Acids↗
PubMedDate not supplied

A comparison of highly unsaturated fatty acid levels in wild and farmed eels (Anguilla anguilla).

1. Absolute and relative amounts of eicosapentaneoic acid (EPA) and docohexaenoic acid (DHA) in muscle of eels from four different fish farms were compared with samples from wild eels from two different areas of northern Italy. 2. Farmed eels were richer in DHA and EPA than wild animals. 3. The addition of cod liver oil to the diet of farmed eels led to a significant accumulation of EPA and DHA, but no change in total lipid content. 4. The calculation of two indices related to highly unsaturated fatty acid (HUFA) content (FLQ = fish lipid quality; AI = aterogenic index), indicated the higher nutritional value of farmed vs wild fish. 5. We conclude that farmed eels are an adequate source of fish products for human nutrition and propose use of the above-mentioned indices as an effective means for assessing fish nutritional quality for populations at high risk of chronic degenerative disease.

Animals↗
PubMed1994

Enoximone inhibits hepatic mitochondrial long-chain acyl-CoA synthetase.

The phosphodiesterase inhibitor, enoximone, was previously shown to cause paradoxical effects on cardiac lipid metabolism. The present study was undertaken to elucidate the effects of enoximone on the hepatic mitochondrial pathway of fatty acid oxidation. Results presented here show that in isolated rat liver mitochondria, palmitate oxidation was inhibited progressively by increasing concentrations of enoximone. Maximum inhibition (35%) of mitochondrial oxygen uptake was attained at 250 microM enoximone. At this concentration, enoximone did not affect the oxidation of either palmitoyl-CoA or palmitoyl carnitine. Also, enoximone did not inhibit the oxidation of the short-chain fatty acid, hexanoate, neither did it affect the respiratory chain in the mitochondria. These data suggest that enoximone specifically inhibits long-chain acyl-CoA synthetase activity. This was confirmed experimentally when the activity of this enzyme was determined in the absence and presence of enoximone. Discovering inhibitors of specific steps in lipid metabolism should provide a useful tool to investigate mechanisms regulating this pathway.

Animals↗
PubMed1985

3-Hydroxyhexanoic acid: an abnormal metabolite in urine and serum of diabetic ketoacidotic patients.

A new organic acid, 3-hydroxyhexanoic acid, was identified in the urine or serum of five diabetic patients with ketoacidosis. The compound was not detected in the urine and serum of healthy subjects or diabetic patients without ketosis. The compound was also detected in the urine of a non-diabetic ketotic patient with dicarboxylic aciduria, suggesting that the occurrence of the compound is more related to the ketotic state than to "diabetic" ketosis.

Caproates↗
PubMed1991

Identification of the main metabolites of 2-ethylhexanoic acid in rat urine using gas chromatography-mass spectrometry.

The metabolites of 2-ethylhexanoic acid, an industrial chemical and the active ingredient in wood preservatives, were investigated in rat urine. Male Wistar rats were given 2-ethylhexanoic acid (2-EHA) in drinking water (600 mg/kg daily) for nine weeks, and then urine specimens were collected and analysed. The compounds were identified by gas chromatography-mass spectrometry in both electron-impact mode and chemical ionization mode. In addition to 2-EHA, ten different 2-EHA-related metabolites were found in the urine of 2-EHA-treated rats. The main metabolite was 2-ethyl-1,6-hexanedioic acid. Urine also contained 2-ethyl-6-hydroxyhexanoic acid and five other hydroxylated metabolites and two lactones, the detailed structures of which have not yet been elucidated. The unsaturated 5,6-dehydro-EHA was also identified; this is the metabolite corresponding to 2-n-propyl-4-pentenoic acid, the hepatotoxic metabolite of valproic acid. At least part of the 2-EHA is present in urine as a glucuronide conjugate.

Animals↗
PubMed1995

Measurement of a new anticonvulsant, (S)-3-(aminomethyl)-5-methylhexanoic acid, in plasma and milk by high-performance liquid chromatography.

A specific and sensitive isocratic method for the measurement of a new anticonvulsant, (S)-3-(aminomethyl)-5-methylhexanoic acid, in rat plasma and milk is described. Following deproteinization, the compound and internal standard [1-(aminomethyl)cycloheptaneacetic acid] were derivatized utilizing 2,4,6-trinitrobenzene sulfonic acid and extracted with cyclohexane. Analytes were resolved on a 5 microns Spherisorb ODSII column (250 mm x 4.6 mm) using a mobile phase of 57% acetonitrile in 0.1 M ammonium acetate, pH 4.0. Absorbance was monitored at 350 nm. Limit of quantitation was 1.00 microgram/ml for a 100-microliters aliquot of plasma or milk.

Animals↗
PubMedDate not supplied

Rates of H2O2 generation from peroxisomal beta-oxidation are sufficient to account for fatty acid-stimulated ethanol metabolism in perfused rat liver.

Fatty acids generate H2O2 via peroxisomal beta-oxidation and increase ethanol metabolism markedly in a system that involves catalase-H2O2. The present studies were conducted to understand why fatty acid-stimulated ethanol metabolism occurs much faster than rates of H2O2 generation reported previously in perfused rat liver. A new method was developed to measure rates of H2O2 generation based on the fact that methanol is oxidized only by catalase in rat liver. Rates of H2O2 generation were estimated from the time necessary for the steady-state level of catalase-H2O2 measured spectrophotometrically (660-640 nm) through a lobe of the liver to return to basal values following the addition of a known quantity of methanol in a closed perfusion system containing 4% bovine serum albumin. Under these conditions, basal rates of H2O2 production and rates of 4-methylpyrazole-insensitive ethanol oxidation were in a similar range (10 to 20 mumol/g/hr). Rates of H2O2 generation were increased up to 80 mumol/g/hr by addition of laurate, palmitate or oleate (1 mM); half-maximal increases in rates were observed with 0.6 mM oleate. Hexanoate, a short-chain fatty acid, did not stimulate H2O2 production or ethanol uptake. In these studies, rates of H2O2 generation compared well with rates of fatty acid-stimulated ethanol uptake measured in the presence of 4-methylpyrazole, an inhibitor of alcohol dehydrogenase, with all fatty acids studied. It is concluded, therefore, that rates of H2O2 generation are sufficient to account for rates of fatty acid-stimulated ethanol metabolism via catalase-H2O2. In addition, these data indicate that catalase may contribute significantly to ethanol oxidation under physiological conditions in the presence of fatty acids.

Animals↗
PubMed1986

Ammonia detoxification by accelerated oxidation of branched chain amino acids in brains of acute hepatic failure rats.

BCAA aminotransferase and BCKA dehydrogenase activities are increased in the mitochondrial fractions from the brains of hepatic failure rats treated with two-thirds removal of CCl4-injured liver. Cerebral leucine decarboxylation was accelerated, and it well correlated with arterial blood ammonia levels. Elevation of brain ammonia content following an intraperitoneal injection of ammonium acetate to hepatic failure rats could be prevented by intravenous infusion of BCAA. Significantly increased brain glutamic acid, glutamine, and alanine contents were noted. These results suggested that accelerated brain BCAA catabolism in acute hepatic failure rats reduce the neurotoxicity of ammonia by promoting the synthesis of glutamic acid and glutamine from BCAA.

Acute Disease↗