Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hypothesis that mictochondrial damage is a significant factor in the pathogenesis of alcoholic liver disease (ALD) was investigated by enzymic analysis of mitochondrial fractions isolated from needle biopsy specimens from control patients, patients with fatty liver due to chronic alcoholism, and from patients with other forms of liver disease. Enzymes associated with the inner and outer mitochondrial membranes showed normal levels in ALD. Enzymes associated with the mitochondrial matrix, glutamate dehydrogenase, malate dehydrogenase and aspartate aminotransferase showed significantly raised levels in ALD, but the levels in patients with non-alcoholic liver disease was normal. In addition, analysis of the mitochondria by sucrose density gradient centrifugation revealed no differences between control tissue and liver from patients with alcoholic liver disease. These results do not indicate that there is significant mitochondrial damage in ALD. The raised mitochondrial matrix enzymes may represent an adaptive response to the ethanol load.
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PMID:Mitochondrial enzyme activities in liver biopsies from patients with alcoholic liver disease. 65 61

Unidirectional air flow isolators were used to house laying hens at 13 degrees C, 18--30 degrees C and 29 degrees C. Their diet was formulated to provide 2655 k cal metabolisable energy/kg and 142 g crude protein/kg. Groups were killed for examination at the age of 35 and 45 weeks. Sub-clinical FLHS occurred in all isolators but in the case of the younger hens appeared to be more prevalent at 29 degrees C than at 13 degrees C. Both the triglyceride and the glycogen content of the liver were higher at 29 degrees C despite a reduction in food intake. The free fatty acid level in the plasma was lower, probably as a consequence of reduced lipolysis. Liver haemorrhage was associated with an increase in plasma aspartate transaminase activity. It was concluded that an interaction between environmental temperature and the energy balance is not the only factor involved in the aetiology of FLHS and maybe of secondary importance, and that there is a pathogenic relationship between hepatic steatosis and haemorrhage.
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PMID:Environmental temperature as a factor in the aetiology of fatty liver-haemorrhagic syndrome in the fowl. 72 32

Fatty liver-haemorrhagic syndrome (FLHS) occurred in the controls and was modified in hens that received a diet containing 10 per cent rapeseed meal. This diet increased the extent and severity of the hepatic haemorrhage without affecting the reticulin content of the liver but decreased the body weight and liver lipid levels and so weakened the correlation between these parameters and haemorrhage score found in FLHS. Plasma aspartate transaminase and beta-glucuronidase activities tended to increase with the score. The rapeseed meal diet also produced thyroid hypertrophy and since this was greater in the hens that produced tainted eggs and was positively correlated with the trimethylamine (TMA) content of the eggs it was postulated that rapeseed meal goitrogens may be involved as secondary factors in producing the disturbance in TMA metabolism that causes the egg taint. This abnormality was associated with a reduction in the soluble protein content of the liver, which reflected a decrease in TMA oxidase activity, but was not related to hepatic haemorrhage, steatosis or reticulolysis, or to lipid levels and the activities of lysosomal enzymes and transaminases in the plasma.
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PMID:Effects of rapeseed meal on laying hens (Gallus domesticus) in relation to fatty liver-haemorrhagic syndrome and egg taint. 74 83

Increased concentrations of neopterin have been found in conditions causing a stimulation of cellular immunity, including various malignancies. In liver diseases, serum or urinary neopterin levels have been studied in acute viral hepatitis, chronic hepatitis, fatty liver and liver cirrhosis. In the present study neopterin serum levels have been measured in 16 patients with hepatocellular carcinoma (HCC), in 32 patients with liver cirrhosis, and in 28 healthy subjects as controls. Mean values of serum neopterin were significantly increased (p < 0.01) in patients with HCC (15.89 +/- 6.34 nmol/l) when compared with those of normal subjects (4.74 +/- 2.13 nmol/l), but no difference was observed between patients with HCC (associated or not with liver cirrhosis) and patients with liver cirrhosis. Neopterin concentrations are not affected by liver cirrhosis aetiology, nor by its clinical severity, and are not correlated to the values of serum alpha-fetoprotein, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, gamma-glutamyl-transferase, and gamma-globulin. The results show that there is a consistent overlap of values in patients with HCC and liver cirrhosis; macrophage activation seems to be a feature of chronic liver diseases, irrespective of HCC development.
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PMID:Serum neopterin levels in patients with hepatocellular carcinoma. 128 21

A protein that has 2 subunits with molecular weight of 35,000 and 23,000 was detected in serum of cattle with hepatic lipidosis (fatty liver). The protein was purified from serum obtained from a cow with fatty liver, and was identified as haptoglobin, which is known to have hemoglobin-binding capacity and to be an acute-phase protein. To assess the relevance of haptoglobin in fatty liver, cattle were classified in 3 groups (healthy control, haptoglobin-positive, and haptoglobin-negative); liver triglyceride content and several serum biochemical variables were evaluated for the 3 groups. Compared with the control and haptoglobin-negative cattle, haptoglobin-positive cattle had significantly (P less than 0.01) higher liver triglyceride content, serum bilirubin concentration, and aspartate transaminase activity. Serum haptoglobin concentration was high in slaughter cattle (27 of 40 cattle tested), particularly in cows (20/28).
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PMID:Purification of a protein from serum of cattle with hepatic lipidosis, and identification of the protein as haptoglobin. 162 86

Using blood chemistry data from 77 cases of hypernutritional fatty liver diagnosed in our gastroenterological clinic, an automated quantitative interpretation was formulated. The reliability of this interpretation was confirmed in view of the following points: 1) Comparison with the degree of fatty infiltration of the liver seen in biopsy specimens or ultrasonographic findings. 2) The high rate of coincidence, sensitivity and specificity among the results. 3) Localization of almost all the cases of fatty or non-fatty liver into circumscribed areas by the value of standard deviation index (SDI) of glutamic oxaloacetic transaminase (GOT) i.e. aspartate aminotransferase (AST) and cholinesterase (CHE), respectively. 4) Graphic display of data and interpretation of a representative case of acute hepatitis at specified stages, and the comparison of this interpretation with clinical diagnoses and course of the disease. Moreover, two possible mechanisms for the elevation of the CHE level were discussed.
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PMID:Interpretation of patho-physiology by laboratory data (4). Cases of hypernutritional fatty liver. 178 Sep 13

During the 26th week of a first pregnancy, a 25-year-old woman presented with pruritus suggesting an intrahepatic cholestasis of pregnancy. The pruritus, however, persisted despite the premature delivery of a normal newborn at the 35th week. Moreover, aspartate aminotransferase activity increased, reaching a maximum of 38 times normal level on the 17th day after the delivery. Thus, an acute fatty liver of pregnancy was suspected and confirmed by liver biopsy. This patient appeared to have both intrahepatic cholestasis of pregnancy and acute fatty liver of pregnancy, an association not previously reported. It is suggested that intrahepatic cholestasis of pregnancy caused premature delivery, which in turn may have prevented the onset of severe maternal and fetal complications caused by acute fatty liver of pregnancy.
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PMID:Intrahepatic cholestasis of pregnancy and acute fatty liver of pregnancy. An unusual but favorable association? 200 12

Albert (Clin Chem 1982;28:1113-9) has proposed estimation of likelihood ratios by logistic regression analysis. The usual likelihood-ratio approach for estimation of post-test probability of disease from sensitivity and specificity data of a diagnostic test has been extended by Birkett (J Clin Epidemiol 1988; 41:491-4) for situations with more than two diagnostic categories. We suggest here a combination of these ideas, demonstrating this by a re-evaluation of previously published data on the validity of neopterin as a tool for differential diagnosis between chronic non-A, non-B hepatitis and fatty liver. Analysis of neopterin data in combination with the ratio between serum concentrations of aspartate aminotransferase and of alanine aminotransferase yielded a good discrimination between three mutually exclusive diagnostic categories, namely, fatty liver and chronic persistent and chronic aggressive non-A, non-B hepatitis. The approach is flexibly applicable to situations with different pre-test probabilities. The sum of estimated post-test probabilities deviates slightly from the sum of pre-test probabilities. This deviation is a function of the coefficients obtained in logistic regression, and an analytical expression for the deviation is given. The generalized likelihood-ratio approach appears promising in complex diagnostic situations when multiple diagnostic tests are available.
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PMID:Generalized likelihood ratio concept and logistic regression analysis for multiple diagnostic categories. 249 33

In order to investigate the reason for the elevation of serum gamma-glutamyltranspeptidase (GGT) after chronic alcohol consumption, the activity of this enzyme, together with the activities of aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase in serum (parameters of liver cell damage) and the excretion of D-glucaric acid (D-GA) in urine (parameter of microsomal enzymatic induction) were determined in 72 chronic alcoholics. Of these, 32 had no significant liver disease (1st group) and 40 had an overt liver disease varying from fatty liver to liver cirrhosis (2nd group). The GGT was elevated in only 62% of the patients of the first group, but in 95% of the second group. Of the latter group, patients with cirrhosis had significantly higher GGT mean levels than the patients with fatty liver. On the other hand, increased D-GA excretion was only found in 23% of the group 1 patients and in 44% of the group 2 patients. Moreover, in all patients there was a significant correlation between the values of GGT and aspartate aminotransferase, but not between GGT and D-GA. From these results, the GGT increase in chronic alcoholics, would seem to be better related to cellular damage than to enzymatic induction assessed on the basis of D-GA urinary excretion.
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PMID:Abnormal serum gamma-glutamyltranspeptidase in alcoholics. Clues to its explanation. 256 72

Persistent abnormalities of liver function tests occur in approximately 15% of home parenteral nutrition (HPN) patients and are associated with steatosis, steatohepatitis, and, rarely, fibrosis or cirrhosis. Approximately one-third of patients with gut failure on long-term HPN have low total and free plasma carnitine concentrations, and it has been suggested that a deficiency of L-carnitine may be responsible for the steatosis and steatohepatitis in HPN patients. To determine whether administration of L-carnitine is capable of reversing steatosis in HPN patients, 4 adult women on HPN for a mean of 53 mo (range 21-80 mo) were studied before and after 1 mo of intravenous L-carnitine supplementation (1 g/day). All patients had abnormalities in standard liver function tests and low total and free plasma carnitine values. The mean total and free plasma carnitine concentrations and the mean total hepatic carnitine concentration were reduced before supplementation and rose to normal values after treatment (27.4 +/- 2.3 to 35.5 +/- 3.1 nmol/ml, 19.4 +/- 2.8 to 25.7 +/- 2.5 nmol/ml, and 3.5 +/- 0.65 to 6.5 +/- 1.2 nmol/mg of noncollagen protein, respectively). However, there were no significant changes in mean serum aspartate aminotransferase and alkaline phosphatase levels (65 +/- 21 vs. 54 +/- 12 IU and 429 +/- 220 vs. 472 +/- 224 IU, respectively), plasma free fatty acids, plasma triglycerides, hepatic free fatty acid and triglyceride concentrations, or the grade of hepatic steatosis on light microscopy. These results suggest that carnitine deficiency is not a major cause of steatosis and steatohepatitis in patients receiving HPN.
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PMID:L-carnitine therapy in home parenteral nutrition patients with abnormal liver tests and low plasma carnitine concentrations. 312 32


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