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)

Previous studies have shown that alpha-tocopherol (vitamin E) pretreatment of experimental animals can protect against acute liver necrosis induced by carbon tetrachloride. In this study we investigated whether the increase of vitamin E liver content by dietary supplementation influences chronic liver damage and cirrhosis induced by carbon tetrachloride in the rat. Our data indicate that vitamin E supplementation did not interfere with the growth rate of the animals and increased about threefold the liver's content of the vitamin. Vitamin E supplementation significantly reduced oxidative liver damage, but it was not effective in protecting against development of fatty liver and did not interfere with metabolic activation of carbon tetrachloride. Moreover, vitamin E-fed animals showed incomplete but significant prevention of liver necrosis and cirrhosis induced by carbon tetrachloride. This has been shown by means of histological examination, analysis of serum parameters and biochemical evaluation of collagen content. These results show that an increased liver content of vitamin E can afford a significant degree of protection against carbon tetrachloride-induced chronic liver damage and cirrhosis.
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PMID:Vitamin E dietary supplementation protects against carbon tetrachloride-induced chronic liver damage and cirrhosis. 139 81

An increase in lipid peroxidation has been found in liver after poisoning with hepatotoxic substances and following dietary changes, i.e. choline-devoid diet and orotic acid-rich diet. In this study we analysed in the rat a model of fatty liver induced by administration of caffeine. The results seem to indicate an increased peroxidability in the liver of caffeine-treated animals, due to an increase in triglyceride content. A decrease of vitamin E which also occurs might contribute to the lipid peroxidation.
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PMID:Lipid peroxidation in fatty liver induced by caffeine in rats. 165 60

Rats were given a 0.05% polychlorinated biphenyls (PCB) diet supplemented with adequate nutrients for 10 days and not only PCB-induced lipid peroxidation as measured by thiobarbituric acid (TBA)-reactive substances but also variations of lipid peroxides scavengers in liver and its subcellular fractions (nuclei and cell debris, mitochondrial, microsomal and cytosolic fractions) were investigated. The lipid peroxidation in liver and subcellular fractions in the PCB-treated group increased significantly except in the nuclei and cell debris fraction. The increase in lipid peroxidation in the microsomal fraction appeared to be associated in part with the decrease in vitamin E (alpha-tocopherol) content and induction of drug-metabolizing enzymes. In the cytosolic fraction, the total lipid content increased, glutathione peroxidase (GSHPx) activity decreased and the quantity of free radical-reactive substances suppressing lipid peroxidation was low as measured by the 1,1-diphenyl-2-picrylhydrazyl (DPPH) value. From these results, the increase in lipid peroxidation in the cytosolic fraction in the PCB-treated group was ascribed to the abundance and availability of oxidizable substrate attended with fatty liver, to the decline in GSHPx activity, and to the insufficiency in antioxygenic activity as observed by the decrease in the DPPH value.
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PMID:Polychlorinated biphenyls-induced lipid peroxidation as measured by thiobarbituric acid-reactive substances in liver subcellular fractions of rats. 212 Dec 82

Spinocerebellar degeneration in a 17-yr-old boy with abetalipoproteinemia was associated with vitamin E deficiency and hepatic steatosis. In liver biopsy samples before and after 15 mo of vitamin E treatment, hepatocellular peroxisomes were morphologically abnormal; pleomorphic, with a broadened range of sizes; often larger than normal; and with marginal bars in some. In the first sample, peroxisomes exhibited matrical heterogeneity and dense nucleoids. Peroxisomes in the second biopsy sample lacked nucleoids and contained more homogeneous matrices. The mean peroxisomal diameter increased from 0.77 +/- 0.33 to 0.86 +/- 0.32 microM (normal, 0.62 +/- 0.14). These observations raise the possibility that peroxisomes may be involved in the metabolism of apolipoprotein B or may be affected by the disturbances of hepatocellular lipid metabolism caused by this disease.
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PMID:Hepatic peroxisomal abnormalities in abetalipoproteinemia. 275 36

Following the pioneer report of Di Luzio (Physiologist 6, 169-173, 1963) concerning the prevention of the acute ethanol-induced fatty liver by antioxidants, many observations have shown that ethanol-induced liver injury may be linked, at least partly, to an oxidative stress resulting from increased free radical production and/or decreased antioxidant defence. The disturbances induced in the major hepatic enzymatic and non-enzymatic antioxidant systems following experimental acute and chronic ethanol administration are reviewed, emphasizing the important role of dietary alpha-tocopherol in modifying the induction of oxidative stress and its usual expression as increased lipid peroxidation. Adaptative increases in some elements of the hepatic antioxidant defence partly counteract the enhanced generation of prooxidant free radicals following chronic ethanol intake. By contrast, lipid peroxidation is favoured when ethanol is administered together with a fat-rich diet and/or various xenobiotics. Chronic ethanol feeding has also been reported to potentiate the oxidative stress resulting from an acute ethanol load. By generating potent chemoattractants for human neutrophils and/or by stimulating the expression of genes involved in collagen biosynthesis, liver lipid peroxidation may play an important role in the progression of steatosis to hepatitis and cirrhosis. Oxidative stress has been shown not to be restricted to the liver, but also to affect, under some experimental conditions of ethanol administration, extrahepatic tissues, such as the central nervous system, the heart and the testes. This stress can be partly prevented by vitamin E supplementation. Ethanol-induced antioxidant disturbances have also been reported in clinical studies in blood and liver biopsies. Pharmacological antioxidants could have beneficial effects in reducing the incidence of ethanol-induced changes in cellular lipids, proteins and nucleic acids. The antioxidants considered could act by reducing free radical production (e.g. chelators of redox-active iron derivatives), trapping free radicals themselves, interrupting the peroxidation process or reinforcing the natural antioxidant defence.
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PMID:Alcohol and antioxidant systems. 781 35

Brown bowel syndrome is a rare intestinal disorder associated with the deposition of lipofuscin pigment in the smooth muscle cells. We report two such cases presenting with intestinal pseudo-obstruction, abdominal pain, and body weight loss. Both cases had malabsorption and fatty liver. Exploratory laparotomy revealed brownish discoloration of the small bowel wall and enlargement of mesenteric lymph nodes. Light microscopy, autofluorescence and ultrastructure studies confirmed the deposition of lipofuscin pigments in the intestinal muscle cells and reticuloendothelial cells of mesenteric lymph nodes. In addition, the calf muscle biopsy of case 1 displayed myopathy and fatty replacement. Skeletal muscle strength of both patients was partially restored after parenteral and oral vitamin E supplement and other conservative treatment, but gastrointestinal symptoms of both patients continued to deteriorate. Thus, brown bowel syndrome associated with prolonged and severe malnutrition and possibly vitamin E deficiency appears only partially responsive to vitamin E supplementation.
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PMID:Brown bowel syndrome: report of two cases. 791 59

The effects of CP and antioxidants on fatty liver hemorrhagic syndrome (FLHS) in Japanese quail hens were studied. In Experiment 1, four treatments were arranged as a 2 x 2 factorial; dietary CP (18 or 24%) and reduced glutathione (GSH, 0 or 120 mg/kg diet) were the major variables, but cysteine and other amino acids were higher in the 24% CP diets. Negative control (NC1) and positive control (PC1) diets were also evaluated. In Experiment 2, the effects of vitamin E (VE) and GSH were evaluated in the presence and absence of adequate dietary sulfur amino acids. Negative control (NC2) and positive control (PC2) diets were used. In both experiments, liver hemorrhage was most severe in quail fed the diets that were formulated to induce hepatic steatosis and limit oxidant defense capability. Liver hemorrhage was least severe in quail fed the diets that were formulated to minimize liver lipid accumulation and support oxidant defenses. Histological evaluation of affected quail livers showed changes consistent with FLHS in chicken hens. In Experiment 1, neither CP concentration nor GSH supplementation influenced liver hemorrhage. In Experiment 2, liver hemorrhagic score was reduced from 3.8 to 2.7 (P < or = .05) by adding VE to the basal diet. The PC2 diet further depressed liver score to only 2.0 (P < or = .05). The data clearly show that Japanese quail are susceptible to FLHS and indicate that a combination of lipotropic and antioxidant nutrients is protective against hemorrhage, even when lipogenic demands are maximized by feeding diets devoid of added fat.
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PMID:Effect of dietary protein and selected antioxidants on fatty liver hemorrhagic syndrome induced in Japanese quail. 826 98

Lipid peroxidation may be important in the pathogenesis of alcoholic liver injury. We investigated the potential of medium chain triglycerides and vitamin E to decrease lipid peroxidation and reverse established alcoholic liver injury. Four groups (five rats/group) of male Wistar rats were studied. Rats in group 1 were fed a fish oil-ethanol diet for 6 weeks. Rats in groups 2, 3 and 4 were fed the fish oil-ethanol diet for 6 weeks before being switched to fish oil-dextrose (group 2), fish oil-dextrose plus vitamin E (group 3) or medium chain triglycerides-dextrose (group 4) diets for 2 weeks. Liver samples were analyzed for histopathology, lipid peroxidation, fatty acid composition and cytochrome P450 2E1 activity. By 6 weeks, all rats developed fatty liver, inflammation and necrosis. After switching to the dextrose-containing diets, there was minimal histologic improvement in group 2, moderate improvement in group 3 and near normalization of the histology in group 4. Histologic improvement was associated with decreased lipid peroxidation and cytochrome P450 2E1 activity. Higher levels of polyunsaturated fatty acids were seen in groups 2 and 3 than in group 4. Our results indicate that a diet enriched in saturated (group 4) but not polyunsaturated (group 2) fatty acids effectively reverses alcoholic liver injury. Treatment with vitamin E also led to histologic improvement. These effects may be explained, at least in part, by down-regulation of lipid peroxidation. Other effects of medium chain triglycerides, such as their propensity for oxidation rather than esterification, may also be important.
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PMID:Medium chain triglycerides and vitamin E reduce the severity of established experimental alcoholic liver disease. 866 40

No published reports compare hepatic alpha-tocopherol (adjusted for hepatic lipid content) with indicators of blood alpha-tocopherol in adult patients with various liver diseases. alpha-Tocopherol was simultaneously measured in liver biopsy tissues and blood from 66 subjects (9 comparison patients hospitalized for biliary tract surgery, 13 with chronic persistent hepatitis, 9 with chronic aggressive hepatitis, 10 with acute hepatitis, 10 with cirrhosis, 7 with both cirrhosis and hepatic cell carcinoma, and 8 with fatty liver). Hepatic, erythrocyte, and plasma alpha-tocopherol concentrations were measured, as were hepatic and serum lipids. The ratios of alpha-tocopherol to total lipid concentrations (Toc/TL ratios) in plasma and liver were calculated. In both comparison patients and patients with chronic persistent hepatitis and fatty liver, hepatic alpha-tocopherol concentrations were strongly correlated with hepatic triglyceride and total lipid concentrations (r = .72, P < .001; and r = .75, P < .001, respectively); the relationships (slopes) when hepatic alpha-tocopherol concentrations were compared with hepatic triglyceride and total lipid concentrations were similar in these patients and in all subjects. No strong correlations were found between hepatic and blood alpha-tocopherol parameters in all subjects. These results suggest that hepatic alpha-tocopherol is present at similar concentrations in triglycerides as well as total cholesterol and phospholipids and that neither plasma Toc/TL ratios nor erythrocyte alpha-tocopherol concentrations are useful indicators of hepatic vitamin E status. The hepatic Toc/TL ratio may be useful to assess total hepatic vitamin E status.
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PMID:Assessment of hepatic vitamin E status in adult patients with liver disease. 925 50

The ability of augmented antioxidant consumption to alter disease incidence, lesion burden and/or longevity was studied in adult male C57BL/6 mice. Mice were fed modified AIN76 diet or modified AIN76 supplemented with vitamin E, glutathione (GSH), vitamin E and GSH, melatonin or strawberry extract starting at 18 months of age. All the mice in this study were heavier than reference populations of male C57BL/6 mice fed NIH-07 or NIH-31, which were maintained without a mid-life change in diet. Fatty liver, focal kidney atrophy and proteinacious casts in the renal tubules were observed more frequently in this study population than in the reference populations. Lesion burden and incidence of specific lesions observed amongst the various groups in this study did not differ. There were no differences observed for longevity of any of the study groups. The longevity observed in this study was similar to that previously reported for male C57BL/6 mice. Thus, diet supplementation with antioxidants initiated during middle age did not appear to affect age-associated lesions patterns, lesion burden or longevity for ad libitum fed male C57BL/6 mice.
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PMID:Disease incidence and longevity are unaltered by dietary antioxidant supplementation initiated during middle age in C57BL/6 mice. 972 3


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