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Biomedical subjects

J Nordmann

Publications and source records attributed to J Nordmann.

At least 55 records · Page 3Linked to original sources
PubMed1977

[Comparison of the effect of acetone and isopropanol on lipid metabolism in rats].

Isopropanol and acetone administered to rats in conditions leading to a similar blood acetone level differ markedly in their effects on lipid metabolism. Isopropanol administration determines a fatty liver, which is mainly related to a defect in hepatic lipoprotein synthesis. Acetone administration gives only raise to a slight increase in the liver triacylglycerol level. It does not alter the [1-14C] palmitate, [1-14C] glycerol or [U-14C] leucine incorporation into blood lipoproteins. Acetone does thus not appear to play a preminent role in the isopropanol induced fatty liver which seems to be related mainly to a direct action of the alcohol itself.

1-Propanol↗
PubMed1977

[Effect of arginine administration on disturbances of hepatic glutamine metabolism during acute ammonia intoxication in the rat].

The present study is concerned with the effects of L-arginine hydrochloride administration on the disturbances of liver glutamine metabolism following acute ammonia intoxication in the rat. Our results show that arginine administration does not suppress the decrease in the hepatic glutamine level and the marked activation of liver glutaminase I induced by ammonia. These alterations do not therefore appear to be related to the limitation of ammonia detoxication through the urea cycle.

Amino Acids↗
PubMed1976

Inhibition of free fatty acid release from isolated rat epididymal fat cells by some natural occurring organic acids.

The effects of some mono-, di- and tricarboxylic substrates (acetate, pyruvate, L-lactate, L-alanine, D,L-beta-hydroxybutyrate, succinate, D,L-malate, alpha-oxoglutarate, L-glutamate and citrate) on the basal lypolytic activity of isolated white adipocytes from fasted rats were investigated "in vitro". At concentrations ranging from 1 to 10 mM, the compounds tested, except lactate, had no influence on the rate of glycerol release but markedly reduced the free fatty acid (FFA) release. Lactate reduced both the glycerol and FFA release. As this "in vitro" lowering effect on FFA release was observed using concentrations occurring "in vivo" in the blood for lactate, beta-hydrobutyrate, and alanine, these results suggest that, besides lactate and beta-hydroxybutyrate, alanine may also assume an important role in the "in vivo" regulation of peripheral FFA mobilization and consequently of ketogenesis.

Adipose Tissue↗
PubMed1976

Is fatty liver induction a general feature of the administration of foreign sulfhydryl compounds?

The intraperitoneal administration of 2-mercaptoethanol or 2-mercaptoacetate (40 muM/100 g body weight) to the rat induces a fatty liver, a marked and early increase of free fatty acids and a decrease of triacylglycerol and phospholipids in the blood. These changes are accompanied by a decrease of the ketone body level and the beta-hydroxybutyrate/acetoacetate ratio in the liver. Under the same experimental conditions, however, administration of 2-mercaptopropionate fails to induce a fatty liver and does not modify the hepatic ketone body level or the blood triacylglycerol and free fatty acid levels. These results led us to conclude that fatty liver induction is not a general feature of foreign thiols, and suggest that increased peripheral fat mobilization as well as decreased hepatic lipoprotein synthesis and/or release are responsible for the 2-mercaptoethanol- and 2-mercaptoacetate-induced fatty liver.

Animals↗
PubMed1976

Influence of pyrazole on hepatic [1-14C] palmitate oxidation during acute ethanol intoxication.

When studied at different times following ethanol intubation, the effects of pyrazole, administered to rats prior to ethanol, affects differently the alcohol-induced disturbances in hepatic [1-14C] palmitate oxidation. This peculiar time-course of the pyrazole induced effects supports the relationship between active ethanol oxidation and inhibition of hepatic fatty acid oxidation, but also emphasizes the caution which must be taken when using pyrazole to study "in vivo" the mechanisms involved in the alcohol induced fatty liver.

Alcoholic Intoxication↗
PubMed1976

[The possible protective effect of cysteine during acute alcohol intoxication].

In the experimental conditions used, cysteine administered per os together with ethanol reduces the blood alcohol levels, but does not modify significantly the rate of alcohol oxidation. No effect of cysteine administration is however observed when ethanol is injected intraperitoneally. Cysteine addition in vitro enhances ethanol consumption by liver slices and reduces at the same time 14CO2 production from [2-14C] ethanol. This effect is only observed with a high cysteine/ethanol molar ratio. The changes in the blood alcohol level resulting from cysteine administration do not appear to result from such an interaction with ethanol oxidation, but seem to be due to a delayed ethanol absorption from the gastrointestinal tract.

Administration, Oral↗
PubMed1976

Influence of aminooxyacetate administration on ammonia-induced metabolic disturbances in the rat liver.

The purpose of the present report was to investigate the effects of aminooxyacetate administration to rats on the ammonia-induced disturbances in the substrate levels and in the activities of the enzymes involved in glutamine metabolism. 1.--Aminooxyacetate enhances the accumulation of ammonia following an ammonia load and prevents the other substrate level changes induced by ammonia. Thus, this transaminase inhibitor suppresses ammonia detoxication by formation of aminoacids as well as by urea synthesis. 2.--A significant decrease of glutamine synthetase activity is observed only after administration of both aminooxyacetate and ammonium chloride. 3.--Like in rats injected with ammonium chloride alone, an ammonia-induced activation of liver glutaminase I is found in inhibitor-pretreated rats. This result confirms the specific enhancement of glutaminase I activity by ammonia in excess.

Acetates↗
PubMed1975

Effect of pyrazole administration on the isopropanol induced fatty liver.

The isopropanol induced fatty liver is prevented in the rat by prior administration of pyrazole. Acetone administration, on the other hand, determines an increase in the hepatic triglyceride level. These results suggest the implications of acetone in the induction of the fatty liver following acute isopropanol administration in the rat.

1-Propanol↗
PubMed1975

Modifications of plasma post-heparin lipolytic activity and tissue lipoprotein lipase activity induced in the rat by acute administration of ethanol or propan-2-ol.

1. The oral administration of propan-2-ol [isopropanol; 100 mmol (6 g)/kg body weight] or ethanol [130 mmol (6 g)/kg body weight] to starved rats produced no change in plasma post-heparin lipase activity (PHLA) compared with that observed in 154 mmol/1 sodium chloride (saline)-treated rats. 2. An increase of adipose tissue lipoprotein lipase (LLA) and a decrease of heart LLA occurred in isopropanol-treated animals, whereas no significant changes were found in these activities after ethanol administration. 3. Since administration of isopropanol produces hyperglycaemia, observations were also made in rats receiving glucose infusion rather than saline. In these animals a rise in PHLA and adipose tissue LLA, and a fall in heart LLA, occurred. 4. It is suggested that the changes in tissue LLA produced by isopropanol are mediated by the rise in blood glucose.

1-Propanol↗
PubMed1975

[Action of isopropanol on rat lipid metabolism: complementary studies on mechanisms implicated in hepatic accumulation of triacylglycerides].

Isopropanol administration (3 g/kg, p.o.) determines in the rat liver an inhibition of fatty acid oxidation, an enhancement of fatty acid esterification into triacylglycerols as well as an inhibition of lipoprotein secretion which appears to be related to alterations in hepatic phospholipids and which differentiates isopropanol from ethanol induced fatty liver. Disturbances in peripheral lipolysis following isopropanol administration are found only in mature rats and are not necessary to the fatty liver induction.

1-Propanol↗