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)

1. Two strains of single comb White Leghorn birds, one susceptible to fatty liver rupture (UCD-003) and a normal commercial strain, were injected with iron nitrilotriacetate and the extent of hepatic lipid peroxidation that occurred was estimated by measuring concentrations of malondialdehyde (MDA). 2. Higher concentrations of MDA were found in the livers of the UCD-003 strain than in the normal birds after injection of iron nitrilotriacetate. No differences were found in the activities of glutathione peroxidase, superoxide dismutase and catalase in the livers of untreated birds of either strain. 3. The degree of unsaturation of the fats in the livers of the two strains was similar. However, the UCD-003 birds had a significantly higher content of liver fat than the normal birds. The increased concentrations of liver fat could account for the increased lipid peroxidation in the UCD-003 birds. 4. The increased incidence of liver haemorrhage that occurs in the UCD-003 birds may be caused by the increased susceptibility of these birds to hepatic lipid peroxidation.
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PMID:Enhanced induction of hepatic lipid peroxidation by ferric nitrilotriacetate in chickens susceptible to fatty liver rupture. 162 19

In order to elucidate active oxygen in liver diseases, activities, electrophoretic profiles and immunolocalization of superoxide dismutase (SOD) in human liver specimens were investigated. Activities and electrophoresis were studied using liver homogenates in 41 cases and immunolocalization of Cu, Zn SOD was observed in 87 cases. Total SOD activity in acute viral hepatitis (AVH) and fatty liver (FL) groups was significantly lower than that in non-specific reactive hepatitis (NSRH) group. Cu, Zn SOD activity in AVH, FL and chronic active hepatitis (CAH) groups was also significantly lower than that in NSRH group. However, no difference of Mn SOD activity, was found between NSRH group and others. Decreased activity of superoxide dismutase in liver tissues suggests the release of this enzyme from the injured hepatocytes. In electrophoretic patterns of superoxide dismutase, 3 bands of Cu, Zn SOD isozymes and 8 to 10 bands of Mn SOD isozymes were recognized. Immunocytochemical investigation revealed the localization of Cu, Zn SOD in the cytoplasm of hepatocytes. Two different distribution of Cu, Zn SOD was observed in the lobules: a diffuse localization pattern and a focal one. The latter was found in the cases of liver diseases with severe parenchymal lesion. These findings suggest that superoxide radical anion and its scavenger, superoxide dismutase, may play an important role in the pathogenesis of liver cell necrosis.
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PMID:Activities, electrophoretic profiles and immunolocalization of superoxide dismutase in human liver specimens. 336 38

The chemiluminescence level and superoxide dismutase (SOD) activity were determined in the plasma of patients with alcoholic and non-alcoholic liver injuries. Chemiluminescence level was significantly higher in alcoholics than in non-alcoholics. It increased significantly in patients with fatty livers and had a tendency to increase with the progression of alcoholic liver injury from a fatty liver to liver cirrhosis. Mn-SOD activity was elevated in patients with alcoholic liver injuries. Furthermore, there was a positive correlation between the levels of plasma chemiluminescence and plasma Mn-SOD activity. The increases in chemiluminescence and Mn-SOD activity suggests that the generation of a large amount of activated oxygen is associated with the pathogenesis and progression of alcoholic liver injury in humans.
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PMID:Chemiluminescence and superoxide dismutase in the plasma in patients with alcoholic and non-alcoholic liver injuries. 402 67

Increased hepatic oxidative stress with ethanol administration is hypothesized to be caused either by enhanced pro-oxidant production or decreased levels of antioxidants or both. We used the intragastric feeding rat model to assess the relationship between hepatic antioxidant enzymes and pathological liver injury in animals fed different dietary fats. Male Wistar rats (5 per group) were fed ethanol with either medium-chain triglycerides (MCTE), palm oil (PE), corn oil (CE), or fish oil (FE). Control animals were fed isocaloric amounts of dextrose instead of ethanol with the same diets. The following were evaluated in each group: liver pathology, lipid peroxidation, manganese superoxide dismutase (MnSOD) levels, copper-zinc SOD (CuZnSOD) levels, glutathione peroxidase (GPX) levels, and catalase (CAT) levels. All enzymes were evaluated using activity assays and immunoblots. Rats fed FE showed the most severe pathology (fatty liver, necrosis, and inflammation), those fed CE showed moderate changes, those fed PE showed fatty liver only, and those fed MCTE were normal. Parameters indicative of lipid peroxidation (conjugated dienes and thiobarbituric acid-reactive substances) were also greater in rat livers from animals fed the diets high in polyunsaturated fatty acids (CE and FE). CuZnSOD, GPX, and CAT activities showed an inverse correlation (r=-.92, P < .01) with severity of pathological injury, with the lowest levels for both enzymes found in FE-fed rats. Decreased enzyme activity in CE- and FE-fed rats was accompanied by similar decreases in immunoreactive protein. Ethanol administration did not cause significant decreases in enzyme activity in groups that showed no necroinflammatory changes (MCTE and PE). MnSOD activity showed no significant change in any ethanol-fed group. Our results show that decreases in CuZnSOD, GPX, and CAT occur in rats showing pathological liver injury and also having the highest levels of lipid peroxidation. These results suggest that feeding dietary substrates that enhance lipid peroxidation can exacerbate both ethanol-induced oxidative damage as well as necroinflammatory changes. The decrease in activity of antioxidant enzymes observed in animals fed diets high in polyunsaturated fatty acids and ethanol could possibly increase the susceptibility to oxidative damage and further contribute to ethanol-induced liver injury.
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PMID:Increased lipid peroxidation and impaired antioxidant enzyme function is associated with pathological liver injury in experimental alcoholic liver disease in rats fed diets high in corn oil and fish oil. 958 86

The modulating effects of selenium-enriched garlic on lipid metabolism disorder and lipid peroxidation were studied in hyperlipidemic rats induced by high fat diet. Adult male and female Wistar rats were divided into 6 groups: (A) normal control; (B) high fat diet (HFD) control; (C) HFD + selenite; (D) HFD + selenium-enriched garlic; (E) HFD + common garlic; (F) HFD + common garlic + selenite. The selenium content of diets in groups A, B and E was 0.08 mg/kg diet, while that of the other 3 groups was 2.7 mg/kg diet. At the end of the experimental period (12 weeks), blood and liver were collected for biochemical measurements and for histopathological examination of liver. The results showed that the serum concentrations of TC, TG and LDL-C in groups C, D and F were significantly lower and HDL-C higher than group B. Female rats were more sensitive to HFD exposure than male rats. The peroxidative status of all four experimental groups was significant inhibited as shown by the lower lipid peroxide (MDA) in liver and higher activities of GPX in erythrocytes and liver and SOD in plasma. Selenium contents in liver and kidney of male rats in groups D and F were higher than group C. Significant accumulation of selenium in erythrocytes was observed in groups D and F. The liver of all four experimental groups revealed ameliorated fatty liver induced by HFD. The amelioration of group D was more prominent than other three experimental groups. The results suggested that selenium-enriched garlic is superior to selenite or common garlic in decreasing the blood lipid level and peroxidative status and slightly better than combined common garlic and selenite.
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PMID:[Effects of selenium-enriched garlic on blood lipids and lipid peroxidation in experimental hyperlipidemic rats]. 1256 39

Hypoxia-inducible factor (HIF) transcription factors respond to multiple environmental stressors, including hypoxia and hypoglycemia. We report that mice lacking the HIF family member HIF-2alpha (encoded by Epas1) have a syndrome of multiple-organ pathology, biochemical abnormalities and altered gene expression patterns. Histological and ultrastructural analyses showed retinopathy, hepatic steatosis, cardiac hypertrophy, skeletal myopathy, hypocellular bone marrow, azoospermia and mitochondrial abnormalities in these mice. Serum and urine metabolite studies showed hypoglycemia, lactic acidosis, altered Krebs cycle function and dysregulated fatty acid oxidation. Biochemical assays showed enhanced generation of reactive oxygen species (ROS), whereas molecular analyses indicated reduced expression of genes encoding the primary antioxidant enzymes (AOEs). Transfection analyses showed that HIF-2alpha could efficiently transactivate the promoters of the primary AOEs. Prenatal or postnatal treatment of Epas1-/- mice with a superoxide dismutase (SOD) mimetic reversed several aspects of the null phenotype. We propose a rheostat role for HIF-2alpha that allows for the maintenance of ROS as well as mitochondrial homeostasis.
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PMID:Multiple organ pathology, metabolic abnormalities and impaired homeostasis of reactive oxygen species in Epas1-/- mice. 1460 55

We studied the effect of administering glycine on tissue lipid peroxidation and enzymic and non-enzymic antioxidants in experimental hepatotoxic Wistar rats. Hepatotoxicity was induced by administering ethanol for 30 days by intragastric intubation. Glycine administered at a dose of 0.6 g kg(-1) body weight for 30 days significantly inhibited the severe oxidative stress as evidenced by the decreased levels of liver and brain thiobarbituric acid reactive substances (TBARS) and hydroperoxides compared to control. The activities of enzymic and non-enzymic antioxidants such as reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) in the liver and brain were significantly elevated on glycine supplementation as compared to the untreated alcohol fed rats. The levels of serum vitamin E and vitamin C were also increased to near normal levels on glycine treatment. Microscopic examination of alcohol treated rat liver showed inflammatory cell infiltrates and fatty changes, which were alleviated on treatment with glycine. Alcohol treated rat brain demonstrated oedma, which was significantly lowered on treatment with glycine. Thus our study shows that administering glycine to alcohol supplemented rats, markedly reduced the oxidative stress and elevated the enzymic and non-enzymic antioxidants in the liver and brain, which a was associated with a reversal of hepatic steatosis and cerebral oedma.
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PMID:Effect of glycine on oxidative stress in rats with alcohol induced liver injury. 1496 23

Great progress has been made in the study of fatty liver with integrated traditional Chinese and western medicine in aspects of diagnosis, treatment and experimental study, etc. Most researches were designed to utilize diagnostic or model replicating method of western medicine to observe the effects or investigate the action mechanism of compound recipe, single Chinese herb or effective ingredients of Chinese herbs on fatty liver. According to the pathological mechanism of traditional Chinese medicine (TCM), fatty liver is characterized by deficiency in nature and repletion in appearance, which involves three Zang viscera such as liver, spleen and kidney and manifests as spleen Qi deficiency, liver and kidney deficiency, phlegm and dampness heaping internally, and Qi stagnation and blood stasis. This facilitates us to use specific recipe or modified recipe to treat fatty liver from the points of integrated traditional Chinese and western medicine and combining syndrome differentiation with disease differentiation. With gratifying achievement, this kind of approach has been the mainstream of the research on fatty liver and many researchers have reached an agreement on this point domestically. Spleen Fortifying and Blood Invigorating Recipe (SFBVER in brief, invented by our institute) can significantly improve the B ultrasound outcome of the liver in patients with fatty liver, with significant difference in B ultrasound scoring between pre-and post-treatment. It can alleviate the patients' symptoms, improve or regain liver function, decrease waist/buttocks ratio and the content of triglyceride and cholesterol in blood. SFBVER is superior to Dongbao Gantai Recipe in general effective rate. Experimental study also reveals that SFBVER can alleviate CCl(4) induced liver cell fatty degeneration and the inflammatory cell infiltration in rats, decrease the activities of ALT and AST, lower the content of triglyceride in liver, recover SOD activity in liver to normal level. The overall efficacy of SFBVER is superior to that of Dongbao Gantai Recipe. Further correlated study should be focused on inventing new preparation of traditional Chinese medicine and investigating its action mechanism with the guiding of the theory of TCM and referring to the latest discovery in fatty liver research in modern medicine.
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PMID:[Studies on treatment of fatty liver with traditional Chinese medicine]. 1533 89

Alcohol is associated with accidental deaths and suicides leading to organ donation, and hepatic steatosis is an important risk factor for initial poor function and failure of human liver grafts. Mechanisms of fatty graft failure are not fully understood, but increased oxidative stress may be a major factor. To characterize the role of free radical stress and the efficacy of antioxidant treatments in fatty liver graft injury, donors for orthotopic rat liver transplantation were treated chronically (3 or more weeks) and acutely (single dose) with ethanol. After transplantation, necrosis and alanine aminotransferase release were threefold to fourfold higher in recipients of fatty grafts from donors treated with ethanol either acutely or chronically compared with findings for recipients of grafts from untreated donors. Moreover, graft survival decreased from nearly 100% to less than 20%. Free radical adducts, as measured by electron spin resonance spectroscopy, were detected in the blood and bile of rats receiving fatty grafts caused by ethanol. Markers of lipid peroxidation also increased after transplantation. Destruction of Kupffer cells with gadolinium chloride decreased free radical production and improved graft survival. Leukocyte adhesion increased beginning early after implantation, and adherent white blood cells obtained from transplanted fatty livers produced the same free radical species as were detected in blood. Therefore, Kupffer cells and adherent white blood cells are important sources of free radicals. Free radicals not only damage fatty grafts directly but also lead to enhanced inflammation and disturbed microcirculation. Delivery of superoxide dismutase-1 and superoxide dismutase-2 genes, free radical-scavenging polyphenols, and antioxidant-containing Carolina Rinse solution reduced injury and improved survival of fatty grafts caused by ethanol. Taken together, these findings indicate that free radicals increase in fatty grafts after transplantation and play an important role in injury of fatty grafts obtained from ethanol-exposed donors. Treatment of fatty donor livers with antioxidants and free radical scavengers may thus be an effective clinical therapy to prevent failure of fatty grafts.
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PMID:Role of free radicals in failure of fatty liver grafts caused by ethanol. 1567 Jun 66

Non-alcoholic fatty liver disease (NAFLD) is emerging as a common medical problem. Nonalcoholic steatohepatitis (NASH) is the critical turning point at which NAFLD progresses to more advanced stages such as hepatic fibrosis, cirrhosis and even hepatocellular carcinoma. However, the study of the pathogenic or therapeutic factors involved in NASH has been hampered by the absence of a suitable experimental model. The aim of the present work was to establish a high-fat emulsion-induced rat model of NASH. Male Sprague-Dawley rats were fed a high-fat emulsion via gavage for 6 weeks. Animals were examined for weight gain, serum and hepatic biochemistry, insulin sensitivity, hepatic malondialdehyde (MDA), superoxide dismutase (SOD) and tissue morphology, as well as cytochrome P-450 2E1 (CYP2E1) and peroxisome proliferator-activated receptor alpha (PPARalpha) expression in the liver. The results showed that rats treated with high-fat emulsion became obese, demonstrated abnormal aminotransferase activity, hyperlipoidemia, hyperinsulinemia, hyperglycemia and insulin resistance. The model rats exhibited an increased concentration of serum TNF-alpha, total cholesterol (TC), triglyceride (TG), MDA and reduced SOD levels in the liver. Immunoblot analysis showed that the expression of CYP2E1 was increased, whereas PPARalpha was reduced in the NASH model rat liver. Moreover, morphological evaluation revealed that hepatic steatosis, inflammation and mitochondrial lesions were also reproduced in this model. In conclusion, a practical and repeatable new rat model of steatohepatitis was established by feeding with high-fat emulsion via gavage. This model provides a valuable research tool and reproduces many of the clinical indices of human NASH.
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PMID:High-fat emulsion-induced rat model of nonalcoholic steatohepatitis. 1662 32


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