Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum DNA polymerase activity (DNA-P) was detected in 27.6 per cent of non-A, non-B (NANB) hepatitis patients, 8.7 per cent of patients with alcoholic liver disease (ALD), 8.6 per cent of hepatitis B surface antigen (HBsAg)-positive patients and 19.0 per cent of HBsAg-negative blood donors with elevated serum glutamic-pyruvic transaminase (SGPT) concentrations. In contrast, none of the patients with hepatitis A, drug-induced liver injury or non-alcoholic fatty liver had DNA-P in their sera in the acute phase of the illness. All HBsAg-positive samples with detectable DNA-P were strongly positive for hepatitis B virus (HBV) DNA, but the samples from patients with NANB hepatitis and ALD and HBsAg-negative blood donors had no HBV DNA. Sensitivity to actinomycin D showed the heterogeneity of DNA-Ps in HBsAg-negative blood donors; the enzyme activity of one type was inhibited by 100 micrograms/ml of actinomycin D, whereas the other was not. The preference for exogenous template primers of these DNA-Ps was different to those of HBV and human retroviruses. The results reveal the prevalence of serum DNA-P in NANB hepatitis patients and suggest that two distinct agents are relevant to the aetiology of NANB hepatitis.
 ...
PMID:Prevalence and heterogeneity of serum DNA polymerase activity in patients with non-A, non-B hepatitis and HBsAg-negative blood donors with elevated SGPT. 212 73

The purpose of this study was to evaluate the clinical diagnostic value of serum total bile acid (STBA) in hepatobiliary diseases. Fasting STBA was measured using the enzymatic colorimetric method in 44 normal control cases and 153 cases of hepatobiliary disease, and then abnormal rates were compared to other conventional liver function tests. These 153 cases of hepatobiliary diseases included acute viral hepatitis (10 cases), chronic persistent hepatitis (32 cases), chronic active hepatitis (16 cases), liver cirrhosis (15 cases), alcoholic hepatitis (11 cases), alcoholic fatty liver (23 cases), alcoholic cirrhosis (17 cases), chronic liver diseases with slight fatty changes (10 cases) and hepatocellular carcinoma (6 cases). Except for 8 cases of acute viral hepatitis, the above cases were verified by liver biopsy. There were also 13 cases of biliary tract diseases. Fasting STBA and other conventional liver function tests were used in the above hepatobiliary diseases during the acute, exacerbated or decompensated stage, and the stable or compensated stage, and their abnormal rates compared. The results of this study revealed that the concentration of STBA is raised in various hepatobiliary diseases, which is related to the degree of hepatic cell injury and the various stages of liver. The concentration of STBA was higher in the acute, exacerbated or decompensated stage than in the convalescent, stable or compensated stage of liver diseases. When the abnormal rates of STBA were compared to other conventional liver function tests, the abnormal rates of STBA were not inferior to r-GT, GOT and GPT, and were more accurate than the other liver function tests.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Diagnostic value of serum total bile acid in hepatobiliary diseases]. 275 25

Compared with controls, patients with alcoholic fatty liver showed a significant increase of gamma-glutamyltransferase activity both in the liver and serum, whereas alkaline phosphatase activity was raised only in the liver but not in the serum. The activities of other enzymes such as aspartate aminotransferase, alanine aminotransferase and glutamate dehydrogenase remained virtually unchanged in the liver of patients with alcoholic fatty liver but were strikingly enhanced in the serum. The hepatic and serum alterations of enzymic activities observed in patients with alcoholic fatty liver could be reproduced in the rat model of alcoholic fatty liver only for gamma-glutamyltransferase but not for the other enzymes tested, substantiating evidence that the animal model may serve as an appropriate tool for studying interactions between alcohol and gamma-glutamyltransferase. The present experiments also indicate that the primary cause for increased serum gamma-glutamyltransferase activities associated with prolonged alcohol consumption is hepatic enzyme induction rather than liver cell injury.
 ...
PMID:Hepatic gamma-glutamyltransferase activity in alcoholic fatty liver: comparison with other liver enzymes in man and rats. 613 56

We measured serum levels of carbohydrate deficient transferrin (CDT) in 420 subjects: 100 healthy blood donors, 82 healthy employees, 70 abstaining patients with different chronic nonalcoholic liver disease, 16 abstaining patients with alcoholic fatty liver, 50 abstaining patients with alcoholic liver cirrhosis, 25 abusing patients with alcoholic fatty liver, 41 abusing patients with alcoholic liver cirrhosis, and 36 patients with alcohol dependence syndrome with a daily ethanol consumption of 173 +/- 120 g the last 4 weeks before blood was drawn. In controls the serum level of CDT was significantly higher in females compared with males (17.7 +/- 5.1 and 13.7 +/- 3.8 units/liter, respectively), and the upper normal limit was defined as 27 and 20 units/liter. Sixty-two of 102 (60.8%) abusing patients with alcoholic liver disease had increased levels of CDT compared with 1 of 66 abstaining (1.5%) patients with alcoholic liver disease, and 10 of 70 (14.3%) abstaining patients with nonalcoholic liver disease among them 3 with primary biliary cirrhosis and 2 with chronic autoimmune hepatitis. No correlation was found between serum CDT and gamma-glutamyltranspeptidase (GGT), AST, ALT, and mean red cell volume (MCV). The sensitivity and specificity for serum CDT was 61 and 92%, respectively, compared with 85 and 18% for GGT and 70 and 66% for MCV. No advantage was gained by using the CDT/transferrin ratio. Our study confirms that CDT is a specific marker for chronic alcohol abuse, except in few patients with other chronic liver diseases. Serum CDT seems to be a better indicator of abstention than GGT; AST and MCV in patients with alcoholic liver disease. However, in our hands CDT is not so sensitive for alcohol abuse in patients with liver disease as reported earlier in unselected alcoholics.
 ...
PMID:Serum carbohydrate-deficient transferrin as a marker of alcohol consumption in patients with chronic liver diseases. 848 62

Propolis designates a mixture of gums, resins and balms, of viscous consistency, which are gathered on certain parts (buds and bark, mainly) of vegetables (especially coniferous trees) by honeybees. They bring this back to the hive, where it is modified and mixed with other substances (essentially their own wax and salivary secretions). In this study, the hepatoprotective and therapeutic effects of propolis ethanol extract on chronic alcohol-induced liver injuries were investigated in rats. 3.125 ml of 99.5% alcohol was added to animal's daily diet for four weeks to induce chronic alcohol liver injuries. After sacrifice, serum transaminases (GOT, GPT), triacylglyceride and hepatic triacylglyceride (HTG) concentration were assayed to observe liver injuries induced by chronic alcohol abuse. In addition, the phenomenon of alcohol induced fatty liver were also observed by histopathological changes. Different doses of propolis ethanol extract were p.o. administered three times per day for three days, after four weeks' alcohol administration. It was found that 10 mg/kg of propolis ethanol extract significantly decreased the elevations of serum GOT, GPT, TG and HTG. In histopathological examination, 30 mg/kg of propolis ethanol extract also remarkably decreased the hepatocellular fatty degeneration, apparent as vacuolization, induced by chronic alcohol abuse.
 ...
PMID:The hepatoprotective and therapeutic effects of propolis ethanol extract on chronic alcohol-induced liver injuries. 935 6

The effects of orally administered dimethyl-4,4'-dimethoxy-5,6,5',6'-dimethylene-dioxybiphenyl-2,2'-d icarboxylate (DDB) on the hepatotoxicity induced by carbon tetrachloride, acetaminophen or ethanol were investigated in rats and mice. Either single or repeated DDB pretreatment (50 or 200 mg/kg) did not alter the hepatotoxicity induced by carbon tetrachloride (0.2 or 1.0 ml/kg, i.p.) in female rats as indicated by increases in the activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and sorbitol dehydrogenase (SDH) in serum. The hepatotoxicity of acetaminophen (350 mg/kg, i.p.) was also unaffected in male mice pretreated with DDB (50 mg/kg/d) for a week. However, DDB administration (50 mg/kg/d for 7 d) decreased the hepatic fatty degeneration induced by repeated ethanol treatment (0.75 g/kg, i.p., x2 times a day for a week) in rats as shown by the accumulation of triglycerides and cholesterol in the liver. Malondialdehyde (MDA) formation in liver homogenates was inhibited by DDB treatment. The significance of the action of DDB on alcoholic fatty liver generation in clinical settings is discussed.
 ...
PMID:Effect of dimethyl-4,4'-dimethoxy-5,6,5',6'-dimethylenedioxybiphenyl-2,2'- dicarboxylate (DDB) on chemical-induced liver injury. 998 71

The aim of the present study was to evaluate the effect of ursodeoxycholic acid (UDCA) on prostaglandin and fatty acid metabolism and the possible relation of these substances to the development of alcoholic fatty liver in rats. The effects of UDCA (40 mg/kg/day, 30 days) were studied in rats pair-fed a high-fat diet (52% of calories as fat) with daily ethanol (4 g/kg/day, 30 days) intragastric intubation. The livers of ethanol-treated animals were characterized by fatty dystrophy. Liver triglyceride and cholesterol ester contents and the activities of serum marker enzymes, alanine aminotransferase and gamma-glutamyltransferase, were significantly increased. Ethanol enhanced phosphoinositol and sphingomyelin content in liver microsomes and lowered prostaglandin E(2) (PGE(2)) concentration in the liver. An increase in the percentage of monoenoic fatty acids and a decrease in the n-6 acid family in liver phospholipids, linoleoyl-CoA desaturase, and PGE(2) synthase activities in liver microsomes were observed in ethanol-treated rats. Treatment with UDCA improved liver morphologic characteristics, decreased triglyceride and cholesterol ester contents, increased the PGE(2) level, and normalized linoleoyl-CoA desaturase and PGE(2) synthase activities, as well as phospholipid and fatty acid patterns in the liver. The activities of the serum marker enzymes were decreased in the ethanol- and UDCA-treated group. Ursodeoxycholic acid lowered the viscosity of the microsomal membrane, as assessed by both fluorescence probe techniques and the saturated/unsaturated fatty acid ratio. We propose that the hepatoprotective effect of UDCA in alcoholic fatty liver is related to the stabilization of microsomal membranes, the prevention of a decrease in essential fatty acids and PGE(2) in the liver, and, probably, an improvement in biochemical processes controlled by PGE(2).
 ...
PMID:Effect of ursodeoxycholic acid on prostaglandin metabolism and microsomal membranes in alcoholic fatty liver. 1174 79

Hepatic steatosis and steatohepatitis are encountered with great frequency in people who consume large amounts of ethanol (more than 6 drinks per day). Ethanol causes steatosis by altering several steps in the hepatic processing of fatty acids, including their uptake from plasma, their use as fuel substrates, and their export as triglyceride. When clinically mild, alcoholic steatosis and steatohepatitis can be difficult to distinguish from nonalcoholic fatty liver disease. This is particularly true among individuals at high risk of accelerated alcoholic liver injury, such as women, the obese, and those with hepatitis C. In the outpatient setting, history and aspartate aminotransferase:alanine aminotransferase ratio offer the best clues to diagnosis. Liver biopsy cannot determine the cause of steatohepatitis, but can show the extent of disease. The etiology of disease is important to prognosis, as alcoholic fatty liver carries a much higher risk of progression and mortality than nonalcoholic fatty liver disease. Patients with moderate to severe alcoholic steatohepatitis are typically hospitalized. Derangements in white blood cell count, prothrombin time, and bilirubin identify those with the highest early mortality. Survival in this severely ill subgroup is improved with the short-term use of corticosteroids; patients who have contraindications to steroids may benefit from other forms of therapy, either pharmacologic, nutritional, or both.
 ...
PMID:Alcoholic steatosis and steatohepatitis. 1194 32

Ob/ob mice, a model for nonalcoholic fatty liver disease (NAFLD), develop intestinal bacterial overgrowth and overexpress tumor necrosis factor alpha (TNF-alpha). In animal models for alcoholic fatty liver disease (AFLD), decontaminating the intestine or inhibiting TNF-alpha improves AFLD. Because AFLD and NAFLD may have a similar pathogenesis, treatment with a probiotic (to modify the intestinal flora) or anti-TNF antibodies (to inhibit TNF-alpha activity) may improve NAFLD in ob/ob mice. To evaluate this hypothesis, 48 ob/ob mice were given either a high-fat diet alone (ob/ob controls) or the same diet + VSL#3 probiotic or anti-TNF antibodies for 4 weeks. Twelve lean littermates fed a high-fat diet served as controls. Treatment with VSL#3 or anti-TNF antibodies improved liver histology, reduced hepatic total fatty acid content, and decreased serum alanine aminotransferase (ALT) levels. These benefits were associated with decreased hepatic expression of TNF-alpha messenger RNA (mRNA) in mice treated with anti-TNF antibodies but not in mice treated with VSL#3. Nevertheless, both treatments reduced activity of Jun N-terminal kinase (JNK), a TNF-regulated kinase that promotes insulin resistance, and decreased the DNA binding activity of nuclear factor kappaB (NF-kappaB), the target of IKKbeta, another TNF-regulated enzyme that causes insulin resistance. Consistent with treatment-related improvements in hepatic insulin resistance, fatty acid beta-oxidation and uncoupling protein (UCP)-2 expression decreased after treatment with VSL#3 or anti-TNF antibodies. In conclusion, these results support the concept that intestinal bacteria induce endogenous signals that play a pathogenic role in hepatic insulin resistance and NAFLD and suggest novel therapies for these common conditions.
 ...
PMID:Probiotics and antibodies to TNF inhibit inflammatory activity and improve nonalcoholic fatty liver disease. 1288 98

The prevalence of and the risk factors for fatty liver have not undergone a formal evaluation in a representative sample of the general population. We therefore performed a cross-sectional study in the town of Campogalliano (Modena, Italy), within the context of the Dionysos Project. Of 5,780 eligible persons aged 18 to 75 years, 3,345 (58%) agreed to participate in the study. Subjects with suspected liver disease (SLD), defined on the basis of elevated serum alanine aminotransferase (ALT) and gamma-glutamyl-transferase (GGT) activity, hepatitis B surface antigen (HBsAg), or hepatitis C virus (HCV)-RNA positivity, were matched with randomly selected subjects of the same age and sex without SLD. A total of 311 subjects with and 287 without SLD underwent a detailed clinical, laboratory, and anthropometrical evaluation. Fatty liver was diagnosed by ultrasonography, and alcohol intake was assessed by using a 7-day diary. Multinomial logistic regression was used to detect risk factors for normal liver versus nonalcoholic fatty liver disease (NAFLD) and for alcoholic fatty liver (AFLD) versus NAFLD. The prevalence of NAFLD was similar in subjects with and without SLD (25 vs. 20%, P = .203). At multivariable analysis, normal liver was more likely than NAFLD in older subjects and less likely in the presence of obesity, hyperglycemia, hyperinsulinemia, hypertriglyceridemia, and systolic hypertension; AFLD was more likely than NAFLD in older subjects, males, and in the presence of elevated GGT and hypertriglyceridemia, and less likely in the presence of obesity and hyperglycemia. In conclusion, NAFLD is highly prevalent in the general population, is not associated with SLD, but is associated with many features of the metabolic syndrome.
 ...
PMID:Prevalence of and risk factors for nonalcoholic fatty liver disease: the Dionysos nutrition and liver study. 1589 1


1 2 3 4 5 6 7 8 9 10 Next >>