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)

5 serum protein polymorphic systems (haptoglobin, alkaline phosphatase, group-specific (Gc) proteins, beta2-glycoprotein 1 and leucine aminopeptidase) and 6 red-cell polymorphisms (adenosine deaminase, adenylate kinase, phosphoglucomutase, glutamic-pyruvic transaminase, phosphogluconate dehydrogenase and acid phosphatase) have been investigated in 54 subjects with tuberous sclerosis. The frequencies of all systems were compared with those of a control sample drawn from a similar mentally retarded population and abnormal distributions were detected in the haptoglobin and Gc system. Quantitative estimation of the serum levels of the Gc protein failed to detect any inter-group differences. Data on the deviations from the Hardy-Weinberg equlibrium, Haldane's Log ratio test between groups, and gene frequencies of both test and control groups are given. It is suggested that selection by mortality is the possible causation for the abnormal distribution of the Gc phenotypes, but the haptoglobin phenotype distribution requires further investigation with care being taken in the selection of control subjects.
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PMID:Serum and tissue proteins in tuberous sclerosis. I. Serum and red-cell polymorphic systems. 16 11

The protective action of aspartic acid on isolated and perfused rat liver was studied. In case of D-galactosamine intoxication the GOT, GPT and SDH activity and the lactate and pyruvate concentration in the perfusion medium were less augmented and the glycogen level in hepatic tissue was less diminished in animals treated with aspartic acid, as compared to controls. The histochemical applied (PAS reaction for glycogen, nucleic acids, NADH2-diaphorase, glucose-6-phosphatase and membrane-ATP-ase), also stated a protecting effect in the treated animals. The protective action of aspartate is hypothetically considered to be exerted by its capacity to reestablish the cellular deficit of pyridine nucleotides and thus to improve the synthesis of nucleic acids, glycoprotein and glycolipids or/and by its participation in various metabolic pathways.
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PMID:Protecting action of aspartate on the hepatic changes induced by D-galactosamine. 18 87

Serum desialylated glycoprotein level was tested for chronic hepatitic patients. The level was significantly elevated in patients with chronic aggressive hepatitis but not in chronic persistent hepatitis comparing to normal subjects. In chronic aggressive hepatitis, severe type (2B), serum desialylated glycoprotein levels were significantly enhanced but not in moderate type (2A) when compared to chronic persistent hepatitis. Sera taken serially from patients with chronic aggressive hepatitis, severe type (2B), demonstrated a slight correlation between circulating desialylated glycoprotein level and serum glutamic-pyruvic transaminase activity.
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PMID:Serum glycoproteins in the liver diseases. V. Desialylated glycoproteins in chronic hepatitis. 74 94

A series of clinical-chemical tests was conducted in 68 schizophrenic out-patients under long-term neuroleptic medication, with particular consideration of the hepatic metabolism, i.e.: Erythrocyte sedimentation rate, alpha 1-glycoprotein, ceruloplasmin, fibrinogen, GPT, GOT, gamma-GT, total protein and serum-protein-electrophoresis. Furthermore, the glucose tolerance tests was carried out. In 44% of the patients an increased erythrocyte sedimentation rate and positive correlations with increased fibrinogen values were found. Increased gamma-GT-values were proven in 33% of the patients; they correlated positively with the increased GPT-and/or GOT-values as well as with pathological glucose tolerance values. Overweight of more than 10 kilos was found in 46% of the patients. A significant correlation between overweight and pathological glucose tolerance values existed. The results were interpreted as consequence of a light fatty liver.
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PMID:[Clinical-chemical studies in schizophrenic out-patients under neuroleptic long-term treatment with particular consideration of the hepatic metabolism (author's transl)]. 88 47

Circulating desialylated glycoprotein level in acute hepatitis was studied by using the competitive binding assay reported by us. Statistically significant differences of the level among acute hepatitis in the peak of illness, fulminating hepatitis and normal subjects were observed. The desialylated glycoprotein level in acute hepatitis was elevated associating with S-GPT and serum bilirubin levels, and it returned to the normal range before S-GPT and serum bilirubin were normalized. The desialylated glycoprotein in a fulminant hepatitis was increasing associated with bilirubin even when S-GPT was decreasing.
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PMID:Serum glycoproteins in the liver diseases. III. Desialylated glycoproteins in the acute hepatitis. 89 34

Alpha-fetoprotein (AFP) is a fetal specific glycoprotein normally produced primarily by the fetal liver. Normally, AFP levels decline rapidly after birth, reaching undetectable levels (less than 10 ng/ml) within several months after birth. The authors have developed a more sensitive radioimmunoassay, which has allowed them to study low levels of AFP in normal adults and to determine factors which may affect its normal level. Two hundred and seventy normal Houston blood donors were screened for the absence of hepatitis B and normal ALT levels. The mean AFP level was 3.04 ng/ml +/- 1.9 SD. There was a statistically significant higher level in men compared to women (p less than .004). Regression analysis demonstrated a statistically significant increase of AFP levels with age both in men (p less than .05) and in women (p less than .01). These data delineate the normal level of serum AFP in normal adults in the United States. With the normal level now defined, it becomes possible to compare levels in different populations including those exposed to hepatotoxins or hepatocarcinogens in the environment.
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PMID:Alpha-fetoprotein levels in normal adults. 137 9

The purpose of this study was to test the hypothesis that different hepatocellular functions are regulated individually during sepsis. This was done by simultaneously measuring bile production, release of liver transaminases, and synthesis of secreted proteins in perfused livers from control and septic rats. Sepsis was induced by cecal ligation and puncture (CLP); control rats were sham-operated. After 16 hours, livers were perfused in situ, and bile flow, synthesis rates of albumin and alpha 1-acid glycoprotein (a major acute-phase protein in rats), and release of glutamic-oxaloacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT) into perfusate were determined. Within the same livers, sepsis resulted in a 54% increase in the synthesis of alpha 1-acid glycoprotein and approximately 30% inhibition of albumin synthesis concomitant with 50% lower bile flow. The concentrations of GOT and GPT in the perfusate increased slightly during the experiments, both when control and septic livers were perfused. The maintained tissue levels of adenosine triphosphate (ATP) and the uptake of Evans blue dye by less than 1% of the hepatocytes, although a late test of viability, suggest that both control and septic livers remained viable during perfusion. The results are consistent with the concept that different hepatocellular functions are individually regulated during sepsis. Thus, impairment of certain hepatocellular functions does not necessarily imply generalized liver failure.
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PMID:Individual regulation of different hepatocellular functions during sepsis. 151 25

The concentrations of human plasma albumin (HPA) and alpha-1-acid glycoprotein (AAG) were measured in the serum obtained from 84 healthy subjects, 56 umbilical cords, 41 patients with renal failure, 65 patients maintained on chronic hemodialysis and 46 patients with liver cirrhosis. Severity of liver dysfunction was assessed with the use of Pugh et al. [1973] classification. Of the cirrhotic patients, 12, 22 and 12 patients were classified as mild, moderate and severe liver dysfunction, respectively. The coefficient of variation of AAG was greater than HPA in all groups of subjects, and the variability of HPA and AAG is increased in patients compared to healthy subjects. As the liver dysfunction progresses, HPA concentration decreases whereas, the average AAG concentration is not changed in mild, moderate and severe liver dysfunction. The coefficients of variation for HPA and AAG in moderate and severe liver disease is over twice those for healthy subjects. The concentration of HPA is normally distributed in all groups of subjects, with the exception of the cord serum. The frequency distribution of AAG was normal in healthy subjects whereas, it was asymmetric, being positively skewed, in newborn, in renal and liver patients. The wide interindividual variability and the not-normal frequency distribution of AAG in liver or renal patients make its mean of little value in defining a group. Neither HPA nor AAG correlated with the clearance of creatinine in renal patients. In liver disease, HPA and AAG did not correlate with GPT and GOT activities, prothrombinic activity and bilirubin concentration. HPA did not correlate with AAG in any group.
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PMID:Interindividual variability in the concentrations of albumin and alpha-1-acid glycoprotein in patients with renal or liver disease, newborns and healthy subjects: implications for binding of drugs. 157 57

Asparagine-linked glycosylation is initiated by the synthesis of N-acetylglucosaminylpyrophosphoryl dolichol (GlcNAc-P-P-dolichol), which is extended by a series of glycosyltransferases to yield Glc3Man9GlcNAc2-P-P-dolichol (where Glc is glucose and Man is mannose). The oligosaccharide unit is then transferred en bloc to asparagine residues of nascent polypeptides in the lumen of the rough endoplasmic reticulum. The question here is whether GlcNAc-P-P-dolichol biosynthesis is a fixed process unaffected by cellular events, or a regulated reaction responsive to cellular requirements for glycoprotein biosynthesis. Several lines of evidence indicate that the latter is the case and that GlcNAc-P-P-dolichol biosynthesis may be subject to multiple forms of regulation. Recent information about the N-acetylglucosamine-1-P transferase (GPT) responsible for this reaction and the cloning of cDNA candidates for this enzyme have provided further insight into these mechanisms. This review will examine current hypotheses dealing with GPT and its role in the committed step of asparagine-linked glycosylation.
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PMID:Biosynthesis of N-acetylglucosamine-P-P-dolichol, the committed step of asparagine-linked oligosaccharide assembly. 166 6

The effect of ischemia on hepatic protein synthesis during sepsis is not known, but is of clinical relevance, since hepatic blood flow decreases during the late phase of sepsis. In this study, synthesis of acute-phase proteins was measured in perfused livers of rats 16 hours after sham operation or cecal ligation and puncture. Livers from each group had 45 minutes of complete ischemia or control perfusion. Protein synthesis was measured during two hour perfusion after the ischemia or control period, by determining incorporation of 3H-leucine into total secreted trichloracetic acid precipitated proteins, immunoprecipitated complement component C3 and albumin and phosphotungstenate-precipitated alpha 1-acid glycoprotein. Lactate, glutamine-oxalacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT) levels in the perfusate were measured during preischemic and postischemic perfusion. Tissue glutathione levels were measured at the end of the perfusion. Synthesis of alpha 1-acid glycoprotein was increased by 100 per cent and albumin synthesis decreased by 46 per cent in septic livers, consistent with an acute-phase response and apparent downregulation of albumin synthesis during early sepsis. Synthesis rates were reduced by 50 to 60 per cent after ischemia in perfused livers from sham operated rats and 70 to 80 per cent in livers from septic rats. Hepatic production of interleukin-1 was not different between the groups during perfusion. GOT and GPT levels increased significantly during ischemia of both nonseptic and septic livers and rapidly returned toward baseline during reperfusion. Lactate levels were higher in perfusate of septic than of nonseptic livers before ischemia and increased further during ischemia. The results suggest that ischemia inhibits production of secreted hepatic proteins similarly in nonseptic and septic livers, but perhaps to a slightly greater extent in septic livers.
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PMID:Effect of ischemia on protein synthesis in the septic liver. 170 61


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