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At least 685 records · Page 38Linked to original sources
PubMed1989

A comparative study of 2-deoxyglucose patterns of glomerular activation in the olfactory bulbs of C57 BL/6J and AKR/J mice.

We have studied the patterns of glomerular activation evoked in the olfactory bulbs of C57BL/6J and AKR/J mice by olfactory stimulations with amyl acetate or isovaleric acid. Patterns of glomerular activation were obtained with the 2-deoxyglucose method and subsequently compared using a computer-assisted image analysis. The mice of both inbred strains stimulated with amyl acetate or isovaleric acid were characterized by areas of high 2-deoxyglucose uptake in their glomerular layer. Statistical comparisons of the patterns demonstrated that they were odor-specific. Although C57BL/6J mice have been found to be specifically anosmic to isovaleric acid, our findings indicate that their olfactory system is topographically activated by olfactory stimulations with this odorant. However, patterns of glomerular activity evoked by isovaleric acid stimulations are not similar in the two studied strains.

Action Potentials↗
PubMed1994

Synthesis of methyl 3-(2-octadecylcyclopropen-1-yl)propanoate and methyl 3-(2-octadecylcyclopropen-1-yl)pentanoate and cyclopropane fatty acids as possible inhibitors of mycolic acid biosynthesis.

(Z)-Tetracos-5-enoic acid is a key intermediate in the biosynthesis of myocobacterial mycolic acids. Recently the methyl ester of its cyclopropene analogue, methyl 4-(2-octadecylcyclopropen-1- yl)butanoate, was shown to act as an inhibitor of mycolic acid biosynthesis. The related analogues methyl 5-(2-octadecylcyclopropen-1-yl)pentanoate and methyl 3-(2-octadecylcyclopropen-1-yl)propanoate have been synthesized, as well as the related cyclopropane esters methyl (Z)-4-(2-octadecylcyclopropan-1-yl)butanoate and methyl (Z)-5-(2-octadecylcyclopropan-1-yl)pentanoate. The synthesis of methyl 3-(2-octadecylcyclopropen-1-yl)propanoate involved protection of the cyclopropene ring by iodination to allow oxidation of an alcohol to a carboxylic acid; the diiodocyclopropane was deprotected by a new mild procedure using activated zinc.

Cyclopentanes↗
PubMed1980

[2-Methyl-3-oxovaleric acid: a characteristic metabolite in propionic acidemia].

Urine samples from 9 patients with propionic acidemis were analyzed with respect to secondary propionyl-CoA metabolites by means of gas chromatography-mass spectrometry. A wide range of variation was observed. The presence of methylcitric and 2-methyl-3-oxovaleric acids, however, was demonstrable in all urines investigated in considerable amounts. For laboratories analyzing urinary organic acids as their methyl esters, 2-methyl-3-oxovaleric acid is considered to be of diagnostic value. In addition to the usual metabolites, the excretion of N-2-methylbutyrylglycine has been demonstrated in the urine of one patient with propionic acidemia.

Amino Acid Metabolism, Inborn Errors↗
PubMed1983

N-Isovalerylalanine and N-isovalerylsarcosine: two new minor metabolites in isovaleric acidemia.

Besides N-isovalerylglycine, isovaleric, 3-hydroxyisovaleric, 4-hydroxyisovaleric, methylsuccinic, mesaconic, 3-hydroxyisoheptanoic and N-isovalerylglutamic acids the excretion of hitherto unreported N-isovalerylalanine and N-isovalerylsarcosine, two minor but characteristic constituents of the organic acid profile in isovaleric acidemia, is described. The new metabolites are assumed to be formed from isovaleryl-CoA by action of the enzyme glycine N-acylase on alanine and sarcosine, respectively.

Alanine↗
PubMed1983

Studies of urinary organic acid profiles of a patient with dihydrolipoyl dehydrogenase deficiency.

Using gas chromatography-mass spectrometry (GC/MS), urinary organic acid profile studies were carried out on a patient with dihydrolipoyl dehydrogenase (E3) deficiency. Elevated levels of 2-hydroxyglutaric acid, 2-hydroxyisocaproic acid and 2-oxoisocaproic acid were observed in addition to lactic acid, 2-oxoglutaric acid, 2-hydroxyisovaleric acid and 2-hydroxybutyric acid previously described in patients with E3 deficiency. The 2-oxoglutaric acid levels were significantly lowered after branched-chain amino acid restriction. In an acute period, the patient was slightly ketoacidotic and excreted larger amounts of 2-oxoglutaric acid and lactic acid than in a static period. It was shown that, prior to confirmatory enzyme studies, patients with E3 deficiency who were suspected to have atypical maple syrup urine disease or chronic lactic acidosis can be rapidly identified by GC/MS analysis of urinary acids.

Caproates↗
PubMed1979

Effect of clofibrate and gemfibrozil on the activities of mitochondrial carnitine acyltransferases in rat liver. Dose--response relations.

The effects of different doses of clofibrate and gemfibrozil on liver size, serum triglyceride concentration and the activities of hepatic mitochondrial alpha-glycerophosphate dehydrogenase (alpha-GPD) and carnitine acyltransferases were studied in male rats. Both clofibrate and gemfibrozil treatment effectively decreased the fructose-induced hypertriglyceridaemia and increased the liver to body weight ratio. Clofibrate treatment also induced an increase of many times in the activities of mitochondrial alpha-GPD and carnitine acyltransferases, the effect increasing with the dose used. The effect of gemfibrozil on the activities of the enzymes was significantly smaller. There was no correlation between the decrease in serum triglyceride concentration and the changes in the activities of the enzymes. Only clofibrate increased the rate of fatty acylcarnitine oxidation in isolated mitochondria. It is concluded that both drugs increased the size of the rat liver, but that only clofibrate influenced the mitochondrial enzyme activities of mitochondrial carnitine acyltransferases and the accelerated mitochondrial oxidation of fatty acids are not the mechanisms by which these drugs lower serum lipid levels.

Acyltransferases↗
PubMed1985

Effect of gemfibrozil on biliary lipid metabolism in normolipemic subjects.

The mechanisms of the lipid-lowering agent gemfibrozil on biliary lipid metabolism were studied in eight normolipemic male volunteers. These measurements were performed before and after 3 months of administration. During administration of gemfibrozil, plasma cholesterol decreased by 19% (P less than 0.01) and triglycerides by 46% (P less than 0.01), and HDL cholesterol increased by 10% (P less than 0.01). The lithogenic index in gallbladder bile increased from 0.73 to 1.37 (P less than 0.05) and in hepatic bile from 0.86 to 1.42 (P less than 0.01). The increase in lithogenicity of gallbladder bile and hepatic bile was due to an increased biliary output of cholesterol from 47 to 70 mg/h (P less than 0.01) and a decreased output of bile acids from 943 to 694 mg/hr (P less than 0.01), whereas phospholipid output was not altered. The reduction in bile acid output was a result of a significant decrease in chenodeoxycholic acid secretion (r = 0.852; P less than 0.01). Cholic acid output was not affected by gemfibrozil. These results suggest that administration of gemfibrozil enhances the possible risk of gallstone formation like clofibrate.

Adult↗
PubMed1982

A pilot study of the effect of Gemfibrozil on some haematological parameters.

In a double-blind 13 week study the effects of Gemfibrozil were compared with placebo. Gemfibrozil was given to 10 patients with evidence of severe atherosclerosis; four similar patients acted as controls. As expected, in the treated group, total cholesterol and triglycerides decreased significantly and HDL cholesterol increased. The Fibrinogen did not change although the ESR increased markedly and the heparin neutralizing activity (HNA) of the plasma decreased (p = 0.01). The antithrombic activity increased. The change in the HNA correlated weakly to the total cholesterol both before and during treatment. These findings show that some of the effects of Gemfibrozil on atherosclerotic humans are similar to those of Clofibrate but others are different.

Aged↗
PubMed1976

Acute functional tolerance to the motor impairment effects of di-n-propylacetate.

Rats were trained to run treadmill fashion along a moving belt to avoid electric shock. After stabilization of performance, the effects of the anticonvulsant di-n-propylacetate (DPA; 100, 200 and 400 mg/kg) on treadmill locomotion were measured. Disturbances in gait and balance were reflected by an increased time off belt in a dose-related manner. In addition, animals showed a progressive improvement over the 3 two-min trials. A second experiment which measured the effects of 300 mg/kg DPA either 5 or 20 min postinjection revealed that the progressive improvement noted in the first experiment was not due to a diminished drug concentration or to an increased exposure to the drug. Thus, acute functional tolerance to the performance decrement produced by DPA appears to depend upon behavioural processes which enable an animal to overcome the drug-induced functional deficit by practicing the task while in the drug state.

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↗
PubMed2006

Chitin and corncobs as electron donor sources for the reductive dechlorination of tetrachloroethene.

Chitin, corncobs, and a mixture of chitin and corncobs were tested as potential electron donor sources for stimulating the reductive dechlorination of tetrachloroethene (PCE). Semi-batch, sand-packed columns were used to evaluate the donors with aerobic and anaerobic groundwaters containing varying degrees of alkalinity. In all experiments, acetate and butyrate were the dominant fatty acids produced, although propionate, valerate, formate, and succinate were also detected. From a multivariable regression analysis on the data, the presence of chitin, limestone, and dechlorinating culture inoculum were determined to be the most positive predictors of dechlorination activity. Chitin fermentation products supported the degradation of PCE to trichloroethene (TCE), cis-1,2-dichloroethene (DCE), and vinyl chloride (VC), even in columns containing PCE DNAPL, whereas dechlorination activity was not observed in any of the columns containing corncobs alone. The longevity and efficiency of chitin as an electron donor source demonstrates its potential usefulness for passive, in situ field applications.

Aerobiosis↗