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)

We previously demonstrated that pulmonary fat embolism was induced by elevation of the core body temperature, in rats with a fatty liver. The aim of the present examination was to investigate the core body temperature at which pulmonary fat embolism developed capillaries through exposure to a high temperature, in rats with a fatty liver. Following heat stress, pulmonary fat embolism was observed to a slight degree at a core body temperature of 41 and 42 degrees C, whereas the severity of pulmonary fat embolism was greatly increased and was classified as severe at a core body temperature of 43 degrees C. Moreover, the concentrations of aspartate aminotransferase and alanine aminotransferase within plasma were significantly increased at a core body temperature of 43 degrees C. These results clearly indicate that the development of pulmonary fat embolism could be related to hyperthermia at above 42 degrees C following heat stress, and that fat emboli may be derived from the fatty liver itself. It is thus likely that pulmonary fat embolism can be considered as one form of evidence of hyperthermia in an individual with a fatty liver.
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PMID:Relationship between pulmonary fat embolism and core body temperature in rats with a severe fatty liver. 1679 13

Steatohepatitis enhances the severity of liver injury caused by acute inflammation. The purpose of this study was to test the hypothesis that fatty liver due to chronic choline-deficient diet exacerbates concanavalin A (ConA)-induced liver hepatitis, which is predominantly facilitated by T cells. Male C57BL/6 mice were fed either control choline-sufficient diet (CSD) or choline-deficient diet (CDD) for 6 weeks before ConA administration. Mice were sacrificed 3, 9, and 24 hours after ConA injection. Liver injury measured by aspartate aminotransferase (AST), alanine aminotransferase (ALT), pathology, and terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) staining was minimal in mice fed either diet before ConA exposure. However, ConA-induced liver injury was significantly greater in CDD-fed mice compared with control-fed mice. Liver cytokines were assessed by quantitative real-time polymerase chain reaction (PCR). The expression of T helper (Th) 1 cytokines tumor necrosis factor alpha (TNF-alpha), interleukin 12 (IL-12), and interferon gamma (IFN-gamma) were dramatically elevated after ConA in CDD-fed mice compared with control-fed mice. CDD also enhanced ConA-induced STAT4 activation, but not STAT6. Notably, regulators of T-cell differentiation were strongly shifted toward a predominant Th1 profile. T-bet, regulator of the Th1 response, was up-regulated in CDD-fed mice, whereas Th2 regulator GATA-3 was significantly suppressed in CDD-fed mice after ConA. Moreover, the expression of suppressor of cytokine signaling (SOCS)-1, SOCS-3, and repressor of GATA-3 (ROG) favored a predominant Th1 cytokine response in CDD-fed mice. In conclusion, these data support the hypothesis that hepatosteatosis caused by CDD is associated with more severe ConA-induced hepatitis due to a predominant shift toward Th1 response.
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PMID:Favored T helper 1 response in a mouse model of hepatosteatosis is associated with enhanced T cell-mediated hepatitis. 1679 67

Nonalcoholic fatty liver disease (NAFLD) is an increasingly recognized condition that may progress to end-stage liver disease, which ranges from simple steatosis to steatohepatitis, advanced fibrosis, and cirrhosis. Oxidative stress and lipid peroxidation are key pathophysiological mechanisms in NAFLD. We investigate the preventive effects of intraperitoneal administration of melatonin (2.5, 5, 10 mg/kg, daily, respectively) in NAFLD rats induced by high-fat diets for 12 wk. Liver damage was evaluated by serological analysis, serum and hepatic lipid assay as well as hematoxylin-eosin staining in liver sections. Oxidative stress and lipid peroxidation were assessed by measuring malondialdehyde (MDA) levels and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in liver. The results showed that high-fat diet induced oxidative stress with extensive liver steatosis in rats. Melatonin (5 or 10 mg/kg) was effective in reducing hepatic steatosis and inflammation with lowering serum alanine aminotransferase, aspartate aminotransferase, and levels liver total cholesterol and triglycerides in high-fat diet rats. Moreover, melatonin (2.5, 5, 10 mg/kg) increased SOD and GSH-Px activities and the 10 mg/kg dose of melatonin reduced MDA levels in liver. This study shows that melatonin exerts protective effects against fatty liver in rats induced by high-fat diet possibly through its antioxidant actions.
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PMID:Melatonin ameliorates nonalcoholic fatty liver induced by high-fat diet in rats. 1684 45

The liver is an important organ closely associated with lipid and glucose metabolism. This study was performed to clarify the relationship between periodontitis and hepatic condition in apparently healthy Japanese women. A cross-sectional study was performed on 172 apparently healthy, dentulous Japanese women (20-59 years old) who attended a health promotion program at Fukuoka Health Promotion Center. After multivariate adjustment for age, smoking history and oral hygiene, which were known risk factors for periodontitis, the incidence of periodontitis (deepest probing depth > or =4 mm) in females was significantly increased with elevated serum levels of aspartate aminotransferase (AST, p < 0.01), alanine aminotransferase (ALT, p < 0.01) and cholinesterase (p < 0.001), and an AST-to-ALT ratio of less than one (p = 0.02). Further adjustment for either body mass index (BMI) or percent body fat did not attenuate these relationships. These results suggest that hepatic steatosis is associated with periodontitis in Japanese women.
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PMID:Relationship between periodontitis and hepatic condition in Japanese women. 1686 98

We investigated the time it took to develop fatty liver and changes in serum aspartate aminotransferase and alanine aminotransferase levels in patients with breast cancer treated with adjuvant tamoxifen. Liver sonography to detect fatty liver and measurement of serum aspartate and alanine aminotransferase levels were performed regularly for patients with early breast cancer. The results were compared in groups of patients with and without adjuvant tamoxifen as well as those on chemotherapy. Eighty-two of 156 patients treated with tamoxifen developed fatty liver, compared with eight of 62 patients not taking it. Fatty liver appeared as early as 3 months after beginning tamoxifen and was detected within 2 years in most cases. It persisted for 48 months after discontinuing tamoxifen in 17 of the 82 patients who developed it. The incidence of fatty liver in patients receiving both chemotherapy and tamoxifen was the same as that in patients receiving tamoxifen alone. While 115 patients had elevations of aspartate aminotransferase, alanine aminotransferase or both, the magnitude of the elevation was clinically significant in only 32 patients. Patients on both chemotherapy and tamoxifen had a higher incidence of elevated transaminases than those on tamoxifen alone. Adjuvant tamoxifen increases the incidence of fatty liver, but has only a minimal effect on aspartate aminotransferase and alanine aminotransferase. Fatty liver may appear as early as 3 months after beginning tamoxifen and may persist for more than 4 years after discontinuing it. Therefore, long-term follow-up is warranted. Chemotherapy is not clearly associated with fatty liver, but may cause a greater degree of hepatocellular damage than does tamoxifen.
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PMID:Fatty liver and transaminase changes with adjuvant tamoxifen therapy. 1691 17

Casein-based diets containing a low (LDI) or high (HDI) dose of soya protein concentrate enriched with isoflavones were fed to obese Zucker rats for 6 weeks. HDI feeding, but not LDI feeding, reduced the fatty liver and decreased the plasma levels of alanine transaminase and aspartate transaminase. This was accompanied by increased activities of mitochondrial and peroxisomal beta-oxidation, acetyl-CoA carboxylase, fatty acid synthase and glycerol-3-phosphate acyltransferase in liver and increased triacylglycerol level in plasma. The decreased fatty liver and the increased plasma triacylglycerol level appeared not to be caused by an increased secretion of VLDL, as HDI decreased the hepatic mRNA levels of apo B and arylacetamide deacetylase. However, the gene expression of VLDL receptor was markedly decreased in liver, but unchanged in epididymal white adipose tissue and skeletal muscle of rats fed HDI, indicating that the liver may be the key organ for the reduced clearance of triacylglycerol-rich lipoproteins from plasma after HDI feeding. The n-3/n-6, 20:4n-6/18:2n-6 and (20:5n-3+22:6n-3)/18:3n-3 ratios were increased in liver triacylglycerol by HDI. The phospholipids in liver of rats fed HDI contained a low level of 20:4n-6 and a high level of 20:5n-3, favouring the production of anti-inflammatory eicosanoids. When obese Zucker rats were fed soya protein, this also resulted in reduced fatty liver, possibly through reduced clearance of VLDL by the liver. We conclude that the isoflavone-enriched soya concentrate as well as soya protein may be promising dietary supplements for treatment of non-alcoholic fatty liver.
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PMID:Dietary soya protein concentrate enriched with isoflavones reduced fatty liver, increased hepatic fatty acid oxidation and decreased the hepatic mRNA level of VLDL receptor in obese Zucker rats. 1692 18

In epidemiological studies, exposure to ambient particulate matter (PM) has been reported to be positively associated with mortality in subjects with diabetes mellitus. Diesel exhaust particles (DEP) are major constituents of atmospheric PM. However, there is no experimental evidence for the relation of DEP to diabetes mellitus and its complications. We investigated the effects of DEP inoculated intratracheally on diabetic changes and nonalcoholic fatty liver disease (NAFLD) in diabetic obese and control mice. db/db mice and the corresponding nondiabetic db/+m mice received exposure to vehicle or DEP every two weeks. Animals were examined with biochemistry, histology, and immunohistochemistry for hexanoyl-lysine (HEL) in the liver. In the db/+m mice, pulmonary exposure to DEP did not increase levels of aspartate aminotransferase (AST) or alanine aminotransferase (ALT) compared to that to vehicle. In the db/db mice, however, the exposure to DEP increased the levels of AST and ALT compared to that to vehicle. Only in the db/db mice, DEP enhanced the magnitude of steatosis and formation of HEL, a marker of oxidative stress, in the liver compared to vehicle. These results suggest that pulmonary exposure to DEP, PM, enhances steatosis in the liver of obese diabetic subjects possibly via enhanced oxidative stress.
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PMID:Pulmonary exposure to diesel exhaust particles enhances fatty change of the liver in obese diabetic mice. 1714 43

The aim of this study was to evaluate the relationship between apolipoprotein E gene polymorphism and nonalcoholic fatty liver disease. The study group consisted of 237 nonalcoholic fatty liver disease patients who were detected by ultrasonography and 201 controls with ultrasonographically normal livers. DNA amplifications were performed by polymerase chain reaction technique and apolipoprotein E genotypes were evaluated after digestion with CfoI restriction enzyme. Serum levels of glucose, lipids, lipoproteins, and apolipoproteins were measured in all subjects. Additionally, viral hepatitis markers, liver enzymes, and body mass index were assessed. Patients were found to have significantly higher triglyceride, glucose, aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyltransferase levels and lower high-density lipoprotein cholesterol and apolipoprotein (a) levels than controls (P<0.05). There were no statistically significant differences in genotypes and allele frequencies between all patients and controls. Comparing nonobese patients with controls, the frequencies of allele epsilon2 and genotype epsilon2epsilon3 were statistically significantly different in the controls (P=0.04 and P=0.01, respectively). In conclusion, occurrence of the epsilon2 allele and epsilon2epsilon3 genotype may be protective against development of nonalcoholic fatty liver disease.
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PMID:Apolipoprotein E gene polymorphism in nonalcoholic fatty liver disease. 1743 74

The present study was conducted to evaluate the hepatoprotective effect of Andrographis lineata (Acanthaceae) extracts in carbon tetrachloride-induced liver injury in rats. Male Wistar rats with chronic liver damage, induced by subcutaneous injection of 50% v/v carbon tetrachloride in liquid paraffin at a dose of 3 mL/kg on alternate days for a period of 4 weeks, were treated with methanol and aqueous extracts of A. lineata orally at a dose of 845 mg/kg/day. The biochemical parameters such as serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase, serum bilirubin and alkaline phosphatase were estimated to assess the liver function. Histopathological studies of the liver were also carried out to confirm the biochemical changes. Histopathological examinations of liver tissue corroborated well with the biochemical changes. The activities of extracts were comparable to a standard drug. Hepatic steatosis, hydropic degeneration and necrosis were observed in the carbon tetrachloride treated group, while these were completely absent in the standard and extract treated groups. A. lineata extracts exhibited hepatoprotective action against carbon tetrachloride-induced liver injury. The present investigation established pharmacological evidence to support the folklore claim that it is used traditionally as a hepatoprotective agent.
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PMID:Hepatoprotective effect of leaf extracts of Andrographis lineata nees on liver damage caused by carbon tetrachloride in rats. 1770 41

Significant disorders of liver metabolic pathways enzymes after high-cholesterol diet could give information on liver steatosis development. This process could probably also be inhibited by some compounds, as examined in rabbits. Forty-two male rabbits were served a high-cholesterol diet (2 g%) (0.67 g/kg b.m./24 h) with addition of d,l-methionine (70 mg/kg b.m./24 h) or seleno-d,l-methionine (12.5 microg/kg b.m./24 h) or alpha-tocopherol (10 mg/kg b.m./24 h) for 3 months to compare the protection effect of used compounds on liver metabolism and steatosis. At the beginning and every month, blood was taken. After the experiment was completed, livers were dissected for histological examinations. The concentration of total cholesterol (t-CH), triacylglycerol (TG), and the activities of aldolase (ALD), sorbitol dehydrogenase (SDH), glutamate dehydrogenase (GLDH), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were determined. Plasma t-CH and TG concentrations were significantly higher in all experimental groups vs control group. Blood serum AST and ALT activities did not undergo change but there were observed not significant increase in the CH group vs control group. Activities of SDH, GLDH, and LDH increased in blood serum and decreased in the liver in all experimental groups. Activities of LDH and SDH increased in the liver in the CH+Met group vs CH group. ALD activity decreased in the liver only in the CH and CH+Se groups. This data support a lipotoxic model of cholesterol-mediated hepatic steatosis. Prolonged administration of high-cholesterol diet not only disturbs the structure of cell membranes, which is expressed by decreased activity of enzymes in the liver and the migration of those enzymes to plasma but as well leads to steatosis of the liver, which has been confirmed by histological examinations. The applied compounds appear to have a varying influence upon the activity of enzymes determined in serum and liver. Obtained results showed a beneficial influence of methionine and vitamin E supplementation on liver steatosis development.
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PMID:The influence of methionine, selenomethionine, and vitamin E on liver metabolic pathways and steatosis in high-cholesterol fed rabbits. 1791 70


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