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At least 1,153 records · Page 64Linked to original sources
PubMed1983

Some comparative effects of gemfibrozil, clofibrate, bezafibrate, cholestyramine and compactin on sterol metabolism in rats.

Liver cholesterogenesis in rats was measured by giving [l-14C]octanoate i.p.; 1 h later digitonin-precipitable sterols were isolated and counted. In rats fed normal chow and given 7 daily p.o. doses of compounds and then fasted, at 20 h after the last dose, clofibrate or bezafibrate had no effect at lower doses or inhibited incorporation at higher doses, while compactin or gemfibrozil caused increases; cholestyramine added to the diet also caused marked increases. When rats were fed chow containing 0.1% cholesterol and 5.5% peanut oil, again at 20 h following the last of 7 daily doses, gemfibrozil caused increases of incorporation which diminished at higher levels of dosage, while clofibrate caused only inhibition. A single dose of gemfibrozil caused inhibition at 3 h postdose followed by increases over control at 36 and 48 h; a single dose of compactin caused inhibition at 3 h but not subsequent increase, and a single dose of clofibrate had no effect over the entire period. In rats fed chow containing 1.5% cholesterol and 5.5% peanut oil, gemfibrozil given orally or cholestyramine in the diet prevented the diet-induced decreases of plasma HDL cholesterol and increases of liver cholesterol content, while bezafibrate treatment did not have those effects. The effects of cholestyramine rapidly disappeared when it was withdrawn from the diet, while the effects of gemfibrozil persisted after dosage was stopped. These results suggest that some of the actions of gemfibrozil on rat sterol metabolism are quantitatively different from those of the other agents tested.

Animals↗
PubMed1983

Role of N-acetylglutamate and acetyl-CoA in the inhibition of ureagenesis by isovaleric acid in isolated rat hepatocytes.

1 and 10 mmol/l isovalerate strongly inhibited urea synthesis in isolated rat hepatocytes incubated with 10 mmol/l alanine and 3 mmol/l ornithine. Isovalerate also markedly decreased N-acetylglutamate levels, and the decrease correlated with the inhibition of urea synthesis by isovalerate. This compound also lowered cellular levels of acetyl-CoA, a substrate of N-acetylglutamate synthase (EC 2.3.1.1). Isovalerate did not significantly affect the cellular levels of ATP and had no direct effect on N-acetylglutamate synthase activity. These results suggest that the inhibition of urea synthesis by isovalerate is due to decrease in N-acetylglutamate levels.

Acetyl Coenzyme A↗
PubMed1978

Glycine therapy in isovaleric acidemia.

The therapeutic efficacy of oral glycine was tested in a 3-year-old girl with isovaleric acidemia. An oral leucine load (25 mg/kg) caused a rise of the blood levels of isovaleric, lactic, and pyruvic acids as well as an increase of urinary excretion of the ketone bodies. These changes did not occur when oral glycine (250 mg/kg) was given with the leucine. Glycine supplementation favored the formation of isovalerylglycine, a nontoxic conjugate of isovaleric acid which is excreted rapidly. Excretion of isovalerylglycine rose threefold when leucine and glycine were administered simultaneously. Chronic glycine therapy was tolerated well and may have prevented one episode of ketoacidosis.

Acidosis↗
PubMed1983

Phenylenebis(oxy)bis[2,2-dimethylpentanoic acid]s: agents that elevate high-density lipoproteins.

A series of phenylenebis(oxy)bis[2,2-dimethylpentanoic acid]s have been synthesized and evaluated as potential hypolipidemic agents. Compound 18 (CI-924) was found to be the most potent compound in this series. In rats, compound 18 not only reduced low-density lipoprotein cholesterol but also increased high-density lipoprotein (HDL) cholesterol. Comparative studies in rats indicated 18 produced an equal elevation of HDL cholesterol at one-third of the dose required of gemfibrozil. Structure-activity relationships are discussed.

Animals↗
PubMed1985

3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors. 1. Structural modification of 5-substituted 3,5-dihydroxypentanoic acids and their lactone derivatives.

A series of 5-substituted 3,5-dihydroxypentanoic acids and their derivatives have been prepared and tested for inhibition of HMG-CoA reductase in vitro. In general, unless a carboxylate anion can be formed and the hydroxy groups remain unsubstituted in an erythro relationship, inhibitory activity is greatly reduced. Furthermore, only one enantiomer of the ring-opened form of lactone 6a(+/-) possesses the activity displayed by the racemate. Insertion of a bridging unit other than ethyl or (E)-ethenyl between the 5-carbinol moiety and an appropriate lipophilic moiety (e.g., 2,4-dichlorophenyl) attenuates activity.

Glycols↗
PubMed1988

Stereoselectivity of rat liver glutathione transferase isoenzymes for alpha-bromoisovaleric acid and alpha-bromoisovalerylurea enantiomers.

The stereoselectivity of purified rat GSH transferases towards alpha-bromoisovaleric acid (BI) and its amide derivative alpha-bromoisovalerylurea (BIU) was investigated. GSH transferase 2-2 was the only enzyme to catalyse the conjugation of BI and was selective for the (S)-enantiomer. The conjugation of (R)- and (S)-BIU was catalysed by the isoenzymes 2-2, 3-3 and 4-4. Transferase 1-1 was less active, and no catalytic activity was observed with transferase 7-7. Isoenzymes 1-1 and 2-2 of the Alpha multigene family preferentially catalysed the conjugation of the (S)-enantiomer of BIU (and BI), whereas isoenzymes 3-3 and 4-4 of the Mu multigene family preferred (R)-BIU. The opposite stereoselectivity of conjugation of BI and BIU previously observed in isolated rat hepatocytes and the summation of activities of enzymes known to be present in hepatocytes on the basis of present data are in accord.

Animals↗
PubMed1987

Helsinki Heart Study: primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia. Safety of treatment, changes in risk factors, and incidence of coronary heart disease.

In a randomized, double-blind five-year trial, we tested the efficacy of simultaneously elevating serum levels of high-density lipoprotein (HDL) cholesterol and lowering levels of non-HDL cholesterol with gemfibrozil in reducing the risk of coronary heart disease in 4081 asymptomatic middle-aged men (40 to 55 years of age) with primary dyslipidemia (non-HDL cholesterol greater than or equal to 200 mg per deciliter [5.2 mmol per liter] in two consecutive pretreatment measurements). One group (2051 men) received 600 mg of gemfibrozil twice daily, and the other (2030 men) received placebo. Gemfibrozil caused a marked increase in HDL cholesterol and persistent reductions in serum levels of total, low-density lipoprotein (LDL), and non-HDL cholesterol and triglycerides. There were minimal changes in serum lipid levels in the placebo group. The cumulative rate of cardiac end points at five years was 27.3 per 1,000 in the gemfibrozil group and 41.4 per 1,000 in the placebo group--a reduction of 34.0 percent in the incidence of coronary heart disease (95 percent confidence interval, 8.2 to 52.6; P less than 0.02; two-tailed test). The decline in incidence in the gemfibrozil group became evident in the second year and continued throughout the study. There was no difference between the groups in the total death rate, nor did the treatment influence the cancer rates. The results are in accord with two previous trials with different pharmacologic agents and indicate that modification of lipoprotein levels with gemfibrozil reduces the incidence of coronary heart disease in men with dyslipidemia.

Adult↗
PubMed1976

The use of pivalic acid as a reference substance in measurements of production of volatile fatty acids by rumen micro-organisms in vitro.

1. A procedure is described for using pivalic acid as an inert reference substance in determination of changes in concentrations of volatile fatty acids (VFA). 2. Pivalic acid in concentrations of up to 80 mmol/1 had no effect on production of methane or VFA by rumen contents. 3. Pivalic acid was inert during incubation with rumen contents from sheep given different diets and with samples taken at different times with respect to feeding.

Acetates↗
PubMed1988

Effects of dietary leucine, alpha-ketoisocaproate and isovalerate on antibody production and lymphocyte blastogenesis in growing lambs.

The chronic effects of oral leucine and leucine metabolites on sheep immune function were determined in two experiments. In replicate experiments, 30 mixed-breed ram lambs were individually fed diets supplemented with approximately 0.05% ruminally protected limestone (control), alpha-ketoisocaproate (KIC), isovalerate (IVA) or leucine (Leu). Serum titers of antibodies produced in response to Brucella abortus antigen and porcine red blood cells were determined. Mitogen-stimulated lymphocyte blastogenesis was determined in experiment 2 by adding phytohemagglutinin (PHA), concanavalin A (Con A) or pokeweed mitogen (PWM) to isolated lymphocytes and measuring [3H]thymidine incorporation. In both experiments, in lambs fed Leu, antibody production to porcine red blood cells was approximately 80% (P less than 0.05) of that in control animals. When KIC was fed, antibody titers to porcine red blood cells were approximately 120% (P less than 0.05) of that of controls. Compared to controls background lymphocyte blastogenesis was higher when KIC was fed, whereas background blastogenesis was lower when Leu was fed (KIC vs. Leu; P less than 0.05). IVA did not significantly affect either measurement. These data indicate that feeding Leu may adversely affect immune function by suppressing lymphocyte activity, whereas oral administration of KIC has a positive influence on immune function in sheep by increasing lymphocyte activity.

Animals↗
PubMed2000

Studies on polyhydroxyalkanoate (PHA) accumulation in a PHA synthase I-negative mutant of Burkholderia cepacia generated by homogenotization.

In the genome of Burkholderia cepacia strain IPT64, which accumulates a blend of the two homopolyesters poly(3-hydroxybutyrate), poly(3HB), and poly(3-hydroxy-4-pentenoic acid), poly(3H4PE), from sucrose or gluconate as single carbon source, the polyhydroxyalkanoate (PHA) synthase structural gene was disrupted by the insertion of a chloramphenicol-resistant gene cassette (phaC1::Cm). The suicide vector pSUP202 harboring phaC1::Cm was transferred to B. cepacia by conjugation. The inactivated gene was integrated into the chromosome of B. cepacia by homologous recombination. This mutant and also 15 N-methyl-N'-nitrosoguanidine (NMG)-induced mutants still accumulated low amounts of PHAs and expressed low PHA synthase activity. The analysis of the mutant phaC1::Cm showed that it accumulated about 1% of PHA consisting of 68.2 mol% 3HB and 31.8 mol% 3H4PE from gluconate. The wild-type, in contrast, accumulated 49.3% of PHA consisting of 96.5 mol% 3HB and 3. 5 mol% 3H4PE. Our results indicated that the genome of B. cepacia possesses at least two PHA synthase genes, which probably have different substrate specificities.

3-Hydroxybutyric Acid↗