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)

The acute effects of the PCB (polychlorinated biphenyls) mixture (Aroclor 1254) on microsomal enzymes and on synthesis and turnover of microsomal and cytoplasmic lipids of rat liver were investigated. Six daily i.p. injections of 25 and 50 mg PCB/kg body weight resulted in increased liver weight and liver to body weight ratios. When compared to controls PCB treatment resulted in a six-fold increase in amount of cytochrome P-450. Activities of NADPH-cytochrome c reductase, ethylmorphine demethylase and inosine diphosphatase were increased whereas glucose-6-phosphatase values were decreased by PCB exposure. Analysis of liver homogenate and microsomal fraction revealed an increase in lipid in PCB-exposed animals. Phospholipids, cholesterol and triglyceride were significantly increased after PCB exposure; however, the greatest percentage increase was seen in the triglyceride pool. The finding of an increase in microsomal triglyceride to phospholipid ratios with exposure to PCB is suggestive of an increase in membrane-enclosed lipid (liposomes). Studies with labelled glycerol indicated that the PCB-induced fatty liver resulted from increased half life but not increased synthesis of liver lipid moieties. The rate of incorporation of leucine into microsomal membrane and albumin was somewhat enhanced in rats exposed to PCB indicative of increased protein synthesis. Morphological studies showed increased occurrence of lipid material, both in cytoplasmic droplets and within rough and smooth-surfaced endoplasmic reticulum. Proliferation of smooth endoplasmic reticulum and flattened Golgi cisternae with no secretion granules containing lipoprotein particles characterized the liver from animals exposed for 6 days. The increase in lipid within membranes of the endoplasmic reticulum together with the flattened Golgi lacking typical secretory vesicles indicates a defect in transport of lipoproteins from the endoplasmic reticulum to the Golgi apparatus and may be the cause of the PCB-induced fatty liver.
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PMID:Studies on the cellular toxicity of polychlorinated biphenyls (PCBs). I. Effect of PCBs on microsomal enzymes and on synthesis and turnover of microsomal and cytoplasmic lipids of rat liver- a morphological and biochemical study. 9 1

Prolactin responses to provocative thyrotropin-releasing factor (TRH) stimulation were evaluated in 43 chronic alcoholic men were divided into groups for analysis based on the presence or absence of gynecomastia and the histologic appearance of their livers as determined by percutaneous liver biopsy. Compared to the normal volunteers, alcoholics with reversible liver disease (fatty liver) had reduced basal prolactin levels and exaggerated TRH responses. In contrast, alcoholics with cirrhosis and gynecomastia had markedly elevated basal prolactin levels and reduced responses to TRH. The results of this study combined with previously reported findings in cirrhotic men provide a basis for a possible explanation for the signs of feminization frequently found in alcoholic men.
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PMID:Hyperprolactinemia and thyrotropin-releasing factor (TRH) responses in men with alcoholic liver disease. 10 34

Retrospective evaluations were made of abdominal echograms in 61 patients who underwent liver biopsy within 3 weeks after ultrasound study. Without knowledge of clinical or biopsy data, determinations were made by two independent observers of: (1) liver size, (2) beam penetration, (3) echogenicity, (4) vascularity, (5) ancillary abnormality, and (6) diagnostic impression. Using these parameters, the presence of generalized parenchymal disease was identified in 81% of reviews of patients with cirrhosis. Thus, in patients with known cirrhosis, there was a 19% false negative rate. In normal patients, 76% were correctly called normal by the reviewers. However, in 24% generalized parenchymal disease was suggested (24% false positive). Patients with fatty liver could not be reliably distinguished from patients with cirrhosis, nor could patients with hepatitis be easily separated from those with normal livers. In all of these determinations, the combination of several features provided more diagnostic accuracy than any single echographic finding.
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PMID:Accuracy of ultrasonography in diagnosis of hepatocellular disease. 11 64

Acute toxicity of individual PCBs, which were categorized as either phenobarbital (PB)- or 3-methylcholanthrene (MC)-type inducers, was examined in young male Wistar rats, comparing their effects on growth rate, organ weight and liver lipid content, 5 days after a single i.p. injection. PB-type PCBs (2,4,3',4'- and 2,5,2'5'-tetrachlorobiphenyl), which slightly increased a content of cytochrome P450, did not show any significant toxicity at a dose of 100 mg/kg. On the contrary, MC-type PCBs (3,4,5,3',4'-pentachloro- and 3,4,5,3',4',5'-hexachlorobiphenyl), which markedly increased a content of cytochrome P448, strongly reduced growth rate and weights of thymus and spleen at a dose of 10 mg/kg. Liver enlargement accompanied by fatty liver was also observed only with MC-type PCBs. 3,4,3',4'-Tetrachlorobiphenyl was also toxic at a dose of 50 mg/kg, in keeping with its weak MC-type-inducing ability. Pretreatment with MC affected neither growth rate, spleen weight, nor liver lipid content. These results suggest that the toxic potency of PCBs is related to their MC-type inducing ability, but the toxic characteristics are different from those of MC itself.
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PMID:Possible correlation between induction modes of hepatic enzymes by PCBs and their toxicity in rats. 11 Jan 91

A placebo-controlled double-blind study of 30 patients with advanced chronic fatty liver was intended to show how far treatment with a liver preparation, in this case Hepavis, is superior to alcohol abstinence alone. Examination of the laboratory parameters, especially of gamma GT shows that treatment with Hepavis with simultaneous withdrawal of alcohol produces a rapid normalization or improvement of the laboratory findings and consequently an accelerated improvement in the course of the disease. This leads to the conclusion that the pathological activity of the liver cell is reduced more quickly by the constituents of Hepavis than without suitable therapy, and that a more favorable prognosis for the fatty liver as a potential precurser of cirrhosis is to be attained. Not only is elimination of the lipogenic factor, alcohol, essential in the treatment of fatty liver, but also treatment with hepatotropic substances.
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PMID:[Treatment of alcoholic toxic fatty liver. A placebo-controlled trial with hepavis (author's transl)]. 11 Oct 85

Monooxygenase enzymes are involved in the biotransformation of drugs and of environmental carcinogens. The activity of 7-ethoxycoumarin 0-deethylase and associated NADPH-cytochrome c reductase was determined in 9000 g supernatant from bioptically obtained liver specimens from patients with various liver diseases in order to study in vitro drug metabolising capacity. Monooxygenase and reductase activity was significantly higher in the livers of 21 patients with alcoholic liver disease (fatty liver, alcoholic hepatitis, cirrhosis of the liver) than in 22 normal controls or in six patients with chronic active hepatitis. The raised activity of drug-metabolising enzymes obtained from alcoholics with liver damage differs from normal values found in five alcoholics without liver disease. Both groups were comparable in respect to the amount of alcohol consumed and duration of abuse. A strikingly low monooxygenase activity was observed in eight patients with cirrhosis of the liver and ascites, with, however, no apparent effect on reductase activity. The results show that alcoholic liver disease is associated with enhanced monooxygenase and reductase activity, but alcoholism, per se, is not. This rise of drug-metabolising enzyme activity could lead to selectively increased rates of biotransformation in patients with alcoholic liver damage.
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PMID:Monooxygenase enzyme activity in alcoholics with varying degrees of liver damage. 11 58

The mechanism of liver enlargement and anti-fatty liver effect of NKK-105 in the rat were investigated by the mesurement of drug-metabolizing enzyme activities and morphological changes in liver tissue detected using electron microscopy. A single administration of NKK-105(250, 500, 1000 mg/kg, p.o.) induced an apparent increase in liver weight. The elevation of aminopyrine demethylase activity and slight increase in microsomal cytochrome b5 and cytochrome P-450 content were seen with the administration of NKK-105. NKK-105 inhibited lipid peroxide formation in mitochondrial and microsomal fractions. Total lipid content of liver decreased at 12 hr after the administration of NKK-105. Lipid peroxide formation in mitochondrial and microsomal fractions was markedly inhibited by the addition of NKK-105 (1 X 10(-3)M), in vitro. Disarrangement of rough endoplasmic reticulum and increase in smooth endoplasmic reticulum were observed by the administration of NKK-105. The decrease in drug-metabolizing enzymes caused by CCl4 or ethionine was protected in the combination with NKK-105. NKK-105 markedly inhibited the elevation of lipid peroxide formation caused by CCl4 or ethionine. Similar effects on lipid peroxide formation were also obtained in vitro. These results suggest that the enlargement induced by NKK-105 indicates a functional not a toxic response. The inhibition of lipid peroxide formation in mitochondrial and microsomal fractions may thus play an important role in the mechanism of anti-fatty liver effect of NKK-105 on the CCl4 or ethionine-induced fatty liver.
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PMID:[Effects of diispropyl 1, 3-dithiol-2-ylidene malonate (NKK-105) on the drug-metabolizing enzymes and fine structure of rat liver (author's transl)]. 12 Feb 99

The results of liver scans performed with 99mTc-sulphur colloid in 169 patients suffering from diffuse liver diseases and in 48 normal controls were evaluated. The patients with reactive hepatitis, acute hepatitis, chronic persistent hepatitis, fatty liver and fibrosis of the liver show only minimal deviations from the scintigraphic pattern. On the contrary, highly increased colloid uptake in the spleen is found in cases of chronic aggressive hepatitis, whilst the intrahepatic distribution of the colloid is approximately normal. In cases of liver cirrhosis, increased colloid uptake is found in the left lobe of the liver as well as in the spleen and in the bone marrow. Either normal findings or cirrhosis-like changes of the colloid distribution are observed in patients with alcoholic hepatitis.
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PMID:[Liver scanning in diffuse liver disease (author's transl)]. 12 69

In 14,744 autopsy cases from an 18-year period 92 cases (of which 7 were ruled out because of decomposition were observed in which death was supposed to be due to direct acute alcoholic intoxication. In the police reports 81 persons were designated as chronic alcoholics or abusers of spirits. The blood alcohol level ranged between 2.04 and 4.92 o/oo. The cases studied were divided into two groups, one with low and the other with high lethal alcohol level. Fatty liver and cirrhosis were found with identical frequency in the two groups, whereas cardiac hypertrophy of obscure origin occurred markedly more often in the group with low lethal blood alcohol level. On the basis the possible mechanism of death in the cases with cardiac hypertrophy is discussed. Finally, the relation between the blood and urine alcohol concentrations observed in 72 cases is discussed. On the assumption that the water phase of the blood was 75 per cent of the total blood, death occurred in the persons without cardiac hypertrophy with fairly identical frequency either in the phase of absorption or the phase of elimination, whereas in the persons with cardiac hypertrophy death most often occurred in the phase of absorption. These statements should, however, be taken with some reservation, partly because the water phase of the blood may vary considerably post mortem (60-90 per cent) and partly because the urine alcohol concentration depends on serval variable factors.
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PMID:[Acute lethal alcohol intoxication (author's transl)]. 13 12

Various aspects of lipid metabolism were examined in broiler chicks affected with fatty liver and kidney syndrome (FLKS). Plasma free fatty acid concentrations were invariably elevated. Plasma triglyceride concentrations were increased amounts of triglyceride-rich lipoproteins. Lipoprotein lipase activity in adipose tissue was considerably reduced, but in heart tissue the enzyme activity was increased. Hepatic lipogenesis was reduced. Rates of oxidation of palmitic and succinic acids by liver, heart and kidney were normal. The increased oxidation rate of palmitic acid following the addition of carnitine was also normal. These findings indicate that elevated blood lipid levels are likely to be an important factor contributing to the development of fatty deposition, particularly in extrahepatic tissues.
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PMID:Some aspects of lipid metabolism in fatty liver and kidney syndrome in chicks. 16 57


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