Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ethanol was found to be capable to stimulate the microsomal xenobiotic-metabolizing enzyme system of human liver. However, this effect was seen only in cases of alcoholic liver damage (fatty liver, alcoholic hepatitis). Alcoholics without alcoholic liver injury had enzyme activities comparable to control patients, who had no liver disease. On ethanol abstinence the enzyme stimulation was reversible within 20 days. Stimulation of xenobiotic-metabolizing enzyme activity in alcoholic liver disease seems to be related to ethanol induced toxicity. The highest enzyme activities were observed in patients on enzyme inducing drugs (2- to 6 fold increase), whereas in alcoholic liver disease enzyme activities were doubled. These results suggest that the stimulation of the microsomal enzyme system caused by ethanol is different from the enzyme induction seen on inducing drugs.
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PMID:[Foreign substance-degrading enzyme system of the human liver. Modification by alcohol, other exogenous factors and liver diseases]. 679 Mar 94

Monkeys (Macaca nemestrina) were divided into four groups, and each group was fed a particular diet. The variables in the diets were as follows: diet A, 0.3 mg cholesterol/kcal nutrient; diet B, 1.0 mg cholesterol/kcal nutrient; diet C, 0.3 mg cholesterol/kcal nutrient, ethanol (36% of calories); diet D, 1.0 mg cholesterol/kcal nutrient, ethanol (36% of calories). Monkeys on the diets containing ethanol developed fatty liver. Mitochondria from ethanol-fed animals demonstrated significant decreases in uncoupler-stimulated, state 3, and state 4 succinate oxidation activity; respiratory control ratio; and ATP content. Liver microsomes isolated from the ethanol-fed groups demonstrated increased ethanol oxidizing activity with either NADPH or H2O2 as cosubstrate. Aniline hydroxylase and aminopyrine-N-demethylase activities were also elevated in ethanol-fed animals. The alterations in these functional properties were related primarily to ethanol in the diets. Cholesterol, while being less of a perturbant than ethanol, did elicit a significant decrease in cytochrome oxidase activity of mitochondria and a small but statistically significant increase in microsomal-associated ethanol oxidation activity. It appeared to potentiate the effect of ethanol in lowering mitochondrial respiratory control and ATP concentrations.
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PMID:Effect of dietary ethanol and cholesterol on metabolic functions of hepatic mitochondria and microsomes from the monkey, Macaca nemestrina. 702 93

The hepatic injury developing during occupational exposure to chemicals was investigated in 23 male patients, aged 23-49 years, by comparing case histories, liver function tests, hepatic microsomal enzyme activities in vivo and in vitro with histology. The subjects, 15 chemical industry workers and 8 painters, had disturbed liver tests after years of exposure to solvents, paints and lacquers. Characteristic for the patients was a 2-4-fold increase in serum aminotransferases associated with normal liver or reactive hepatitis with or without fatty liver. All patients, except subjects with fatty change, had metabolically active liver which was reflected as adaptive and toxic changes in cellular ultrastructure. The biochemical liver tests normalized within 3-6 weeks after cessation of the exposure. The findings demonstrate that occupational exposure to chemical solvents may insidiously damage the liver. The injury is detectable by biochemical, metabolic and histological investigations in the early phase.
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PMID:Liver injury in subjects occupationally exposed to chemicals in low doses. 714 16

The therapeutic effect of diisopropyl 1,3-dithiol-2-ylidenemalonate (NKK-105) on the fatty liver induced by carbon tetrachloride (CCl4) was studied. The recovery from elevated liver triglyceride levels induced by CCl4 required over 20 days in 35 week-old rats, but 14 days in 6 week-old rats. This indicates that 35 week-old rats are useful for studying the therapeutic effect of NKK-105 on fatty liver. In rats with CCl4-induced fatty liver, NKK-105 lowered the hepatic triglyceride level, accelerated the rate of triglyceride release from the liver, enhanced the incorporation of 14C-leucine into microsomal protein, and increased the RNA content in microsomes. These data suggest that NKK-105 exerts a curative effect on CCl4-induced fatty liver by improving the impaired protein synthesis and by promoting lipoprotein secretion.
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PMID:Effect of diisopropyl 1,3-dithiol-2-ylidenemalonate (NKK-105) on fatty liver induced by carbon tetrachloride. 725 41

The rat liver mixed function oxydases are induced by polychlorocamphane incorporated in the food at a dose level of 250 ppm for 30 days. The fat content of liver is enhanced by the treatment, specially that of microsomal phospholipids and whole liver esterified cholesterol and triglycerides. Microsomal acylcoenzymeA-cholesterol-acytransferase activity, expressed in nM/g of liver weight, which catalyses the esterification of free cholesterol, is increased significantly by P.C.C. treatment. The accumulation of triglycerides is inconsistent with an enhanced lipolysis of adipose tissue since the plasma levels of free fatty acids are the same for control and treated rats. These results confirmed the eventual correlation between induction and hepatic steatosis suggested by some authors.
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PMID:[Polychlorocamphane (P.C.C.) effects on the microsomal enzyme activities and fat content of rat liver (author's transl)]. 728 Nov 66

Hepatic drug-metabolizing capacity was investigated in 56 diabetics. The antipyrine test was selected as an in vivo index, since its kinetics indirectly reflect the metabolically active liver mass. Hepatic cytochrome P-450 (P-450), determined from the biopsy samples, was used as an in vitro parameter, since it is a direct measure of microsomal drug-metabolizing enzyme activity. There was a wide interindividual variation in the indexes of drug metabolism in the diabetics: 40 fold in P-450 content and eightfold in antipyrine metabolism. P-450 levels were higher and antipyrine metabolism faster in the subjects with normal liver than in those with fatty liver, parenchymal inflammatory changes, or cirrhosis. Thus the in vivo and in vitro parameters of drug metabolism were related to the alterations in liver histology. On the other hand, the diabetes per se did not seem to alter the drug-metabolizing capacity of the liver. Also, drug metabolism in diabetics classified by treatment regimen did not differ significantly.
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PMID:The evaluation of the drug-metabolizing capacity in patients with diabetes mellitus. 743 38

The hypocholesterolemic action of eritadenine, a compound found in the mushroom Lentinus edodes, was investigated in relation to its influence on phospholipid metabolism in the liver of rats fed diets containing different amounts of choline chloride (0, 2 and 8 g/kg diet). The time-dependent effect of eritadenine supplementation was also investigated. Eritadenine supplementation (50 mg/kg diet) significantly decreased the phosphatidylcholine (PC):phosphatidylethanolamine (PE) ratio in liver microsomes and the S-adenosylmethionine (SAM):S-adenosylhomocysteine (SAH) ratio in the liver, in addition to the plasma cholesterol concentration, irrespective of dietary choline levels. There was a significant correlation between the plasma cholesterol concentration and the liver microsomal PC:PE ratio. Although eritadenine caused fatty liver when added to the diets containing 0 or 2 g/kg choline chloride, a high level (8 g/kg) of choline chloride fully prevented the eritadenine-induced fatty liver without diminution of hypocholesterolemic action. Both the PC:PE ratio and the SAM:SAH ratio decreased significantly prior to the decrease in the plasma cholesterol concentration (1 d vs. 2 d after) in response to eritadenine supplementation, supporting the hypothesis that the alteration of hepatic phospholipid metabolism may be a cause of the hypocholesterolemic action of eritadenine. These observations suggest that the essential hypocholesterolemic action of eritadenine might be associated with a modification of hepatic phospholipid metabolism rather than with the PC deficiency, due to the inhibition of PE N-methylation.
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PMID:Hypocholesterolemic action of eritadenine is mediated by a modification of hepatic phospholipid metabolism in rats. 764 48

Liver fatty acid-binding protein (L-FABP) expression is modulated by developmental, hormonal, dietary, and pharmacological factors. The most pronounced induction is seen after treatment with peroxisome proliferators, which induce L-FABP coordinately with microsomal cytochrome P-450 4A1 and the enzymes of peroxisomal fatty acid beta-oxidation. These effects of peroxisome proliferators may be mediated by a receptor which has been shown to be activated by peroxisome proliferators in mammalian cell transfection studies. However, the peroxisome proliferators tested thus far do not bind to this receptor, known as the peroxisome proliferator-activated receptor (PPAR), and its endogenous ligand(s) also remain unknown. Peroxisome proliferators inhibit mitochondrial beta-oxidation, and one hypothesis is that the dicarboxylic fatty acid metabolites of accumulated LCFA, formed via the P-450 4A1 omega-oxidation pathway, serve as primary inducers of L-FABP and peroxisomal beta-oxidation. We have tested this hypothesis in primary hepatocyte cultures exposed to clofibrate (CF). Inhibition of P-450 4A1 markedly diminished, via a pre-translational mechanism, the CF induction of L-FABP and peroxisomal beta-oxidation. In further experiments, long-chain dicarboxylic acids, the final products of the P-450 4A1 omega-oxidation pathway, but not LCFA, induced L-FABP and peroxisomal beta-oxidation pre-translationally. These results suggest a role, in part, for long-chain dicarboxylic acids in mediating the peroxisome proliferator induction of L-FABP and peroxisomal beta-oxidation. We also found that LCFA, which undergo rapid hepatocellular metabolism, could become inducers of L-FABP and peroxisomal beta-oxidation under conditions where their metabolism was inhibited.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of regulation of liver fatty acid-binding protein. 823 72

Arsenazo III (AIII) (100 mg/kg ip in saline) administration to Sprague-Dawley male rats 30 min before or 6 or 10 hr after CCl4 [1 ml/kg ip as a 20% (v/v) solution in olive oil] significantly prevented liver necrosis but not fatty liver caused by the hepatotoxin at 24 hr as demonstrated either by histology or by determination of isocitric acid dehydrogenase in plasma. AIII did not modify the CCl4 concentrations reaching the liver, the intensity of the covalent binding of CCl4-reactive metabolites to hepatic microsomal lipids, or the CCl4-promoted lipid peroxidation process at either 1 or 3 hr of poisoning. AIII administration enhanced glutathione (GSH) levels in liver and significantly prevented the CCl4-induced minor decreases in GSH content and the CCl4-induced increases in calcium content at 24 hr of intoxication. AIII treatment further enhanced the CCl4-induced decreases in body temperature of the poisoned rats. Results suggest that AIII's preventive effects might be related to its very well-known calcium-chelating properties, but that additional factors related to AIII's ability to increase GSH content in liver or to decrease body temperature of CCl4-intoxicated animals may also play a role.
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PMID:Prevention of CCl4-induced liver necrosis by the calcium chelator arsenazo III. 851 46

We have previously demonstrated that low-casein diets supplemented with cystine and threonine reduced hyperlipidemia and proteinuria in nephritic rats without noticeable protein malnutrition. In the present study, we examined whether or not a low-casein diet supplemented with methionine, sulfur amino acid other than cystine, and threonine would ameliorate the symptoms without protein malnutrition in rats with nephrotoxic serum nephritis by feeding experimental diets for 10 days. A methionine-threonine-supplemented 8.5% casein diet (8.5 CMT), when compared with a basal 20% casein diet, improved hypoalbuminemia as well as hyperlipidemia and proteinuria without noticeable growth retardation and fatty liver induction in nephritic rats. Fecal bile acid excretion and microsomal cholesterol 7 alpha-hydroxylase activity were enhanced by 8.5CMT feeding. These results suggest that amino acid-balanced low protein diet would have a beneficial effect on the symptoms of nephritis. They also suggest that the hypocholesterolemic action of 8.5CMT may be, at least in part, due to increased fecal bile acid excretion accompanied by elevated microsomal cholesterol 7 alpha-hydroxylase activity.
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PMID:Improvement of hyperlipidemia and proteinuria without noticeable growth retardation by feeding a methionine and threonine supplemented low-casein diet to nephritic rats. 853 82


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