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)

I. In three separate experiments, four groups of five to eight young male rats were fed either (i) a high-protein diet, for which the net dietary protein:total metabolizable energy ratio (NDp:E) was 0-1 (HP diet); or (ii) a low-protein diet, for which NDp:E was 0-04 (LP diet). In both these groups, food intake was ad lib. In group (iii) the HP diet was given in an amount approximately equal to that taken by the LP group fed ad lib. (HP-restricted). In group (iv) rats were fasted for 48 h after receiving the HP diet (HP-fasted). Each experiment lasted 4 weeks. 2. In the LP and HP-restricted groups, food intake was about 50% of that of the HP rats, while body-weight, after 4 weeks on diet was about 35% and 55% of that of HP rats, for LP and HP-restricted respectively. Both groups of malnourished rats gained some weight during the experiment. 3. Measurements of oral glucose tolerance and plasma insulin levels were made in the fourth week. LP and HP-restricted rats both showed low fasting insulin levels and low insulin to glucose ratios during the glucose tolerance tests; the LP rats were more seriously affected. 4. At the end of the fourth week the rats were killed and blood, liver and gastrocnemius muscle were analysed. LP rats showed specifically and consistently low values for haemoglobin and plasma protein concentration, and low activities of hepatic glucose-6-phosphatase (EC 3-1-3-9) and of alanine aminotransferase (EC 2.6.1.2) in liver and muscle. The activity of hepatic aspartate aminotransferase (EC 2.6.1.1) was, if anything, increased. The plasma amino acid concentrations and ratios showed a specific fall in branched-chain amino acids. Liver fat concentration was consistently elevated. The HP-restricted rats had normal values for haemoglobin, plasma protein andliver fat, and near-normal values for plasma amino acids. Hepatic alanine aminotransferase showed increased activity compared with HP rats, but muscle alanine aminotransferase showed reduced activity. The HP-fasted rats had increased haemoglobin, plasma protein and liver fat concentration, and very low liver glycogen concentrations. Hepatic alanine aminotransferase activity was elevated. Plasma alanine concentration was specifically reduced. 5. The results are consistent with suppression of gluconeogenesis, liver dysfunction and essential amino acid deprivation in LP rats. These biochemical changes found in rats on a low intake of a diet of low protein and high carbohydrate value are similar to those found in kwashiorkor. An equally low intake of a diet of good protein value (HP-restricted) led to marginally better growth, accompanied by biochemical signs of increased gluconeogenesis, analogous to those reported for nutritional marasmus. This nutritional state was not biochemically identical with that of acute fasting. 6. The results are discussed in terms of the consistency of the rat model, and its contribution to understanding biochemical changes found in infant malnutrition.
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PMID:Biochemical characteristics of different forms of protein-energy malnutrition: an experimental model using young rats. 40 28

A marginal protein malnutrition model which makes allowances for the increasing nutritional requirements of the growing rat and the effects of dietary manipulation on diurnal rhythms, while still rigidly controlling the level of protein restriction, is reported. A predetermined, constantly increasing intake of four purified diets, providing approximately 40 to 160% of the National Research Council protein requirement for rats was fed to rats receiving a nitrogen-free energy source adlibitum. This standardization reduced within-group variation and allowed precise growth reproducibility. Biochemical parameters were measured at evenly spaced intervals throughout the day to remove diurnal differences from between-group comparisons. Growth, nitrogen balance, and 24-hour means of liver weight, DNA, RNA, protein, and glutamate-oxaloacetate and glutamate-pyruvate transaminases reflected protein intake. However, when growth was depressed 10, 30, or 60%, liver GPT/DNA was depressed 40, 49, or 67%, respectively. Hepatic GPT appears to be a sensitive and accurate indicator of marginal protein malnutrition.
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PMID:Hepatic transaminase in protein-restricted rats: development of a controlled model. 56 97

Two patients with anorexia nervosa with evidence of pancreas and liver injury are reported. Both showed evidence of organ dysfunction in the presence of cachexia. Serum amylase, ASAT (GOT), and ALAT (GPT) became normal parallel with body weight. On the basis of reports on the effects of malnutrition on pancreas and liver function, it is suggested that nutritional pancreas and liver dysfunction might represent hitherto unrecognized complications of anorexia nervosa.
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PMID:Hepatic and pancreatic dysfunction in anorexia nervosa: a report of two cases. 58 48

Serum and urinary RNase activity was determined in 15 normal children and in 52 children in various clinical stages of schistosomal hepatic fibrosis. The activity of serum RNase was compared with that of serum GOT, GPT and AP. The activity of serum and urinary RNase in the different schistosomal groups was significantly higher than in healthy children. The elevated levels of serum and urinary RNase activity were possibly due to malnutrition with tissue catabolism, zinc-deficiency and liver cell injury. Treatment with Astiban and protein-rich diet resulted in a significant decrease in serum and urinary RNase activity and an in significant drop in serum GOT, GPT and AP. Serum and urinary RNase appear to be more sensitive indices for evaluating the early metabolic disturbances in schistosomal patients than GOT, GPT or AP. Our findings also showed that the severity of cases could be graded according to the level of urinary RNase.
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PMID:Serum and urinary ribonuclease in children with schistosomal hepatic fibrosis. 73 20

This paper reports a study of changes in red blood cell enzymes and some serum parameters during and after treatment of protein-calorie malnutrition. The red cell GSH levels were low during the crisis, together with the levels of GSSG:NADPH reductase, GSH:H2O2 peroxidase, aspartate aminotransferase and alanine aminotransferase. After treatment the levels of all these enzymes increased significantly to normal values. Of the serum parameters investigated, significant reduction in the activity of the enzymes cholinesterase, catecholamine oxidase, total proteins, albumin, urea and electrolytes were obvious, and returned to normal values after treatment. Ceruloplasmin activity remained low even after three weeks' treatment and could not be related to copper levels. The results are discussed in relation to anemia and liver damage that may accompany the syndrome.
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PMID:Protein-calorie malnutrition: a study of red blood cell and serum enzymes during and after crisis. 82 Apr 94

Twenty-six 3-week-old genetically obese pigs were fed in two experiments to determine the serum chemistry profile during severe protein malnutrition and repletion. Severe protein deficiency was produced in pigs fed the high-fat, low-protein diet (growth failure, rough hair, low serum total protein and albumin). In Experiment 1, blood was sampled from the anterior vena cava of each pig five times during depletion and three times during repletion to determine serum total cholesterol, high density lipoprotein (HDL)-cholesterol, triglycerides, total protein, albumin, glucose, Ca, inorganic P, Mg, Na, K, Cl, total bilirubin, urea N, creatinine, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyltransferase. In Experiment 2, blood was sampled weekly for 8 weeks for serum total cholesterol, HDL-cholesterol, triglycerides, albumin, glucose, Ca, P, Mg and alkaline phosphatase. HDL-cholesterol was increased (P less than 0.01) and albumin was decreased (P less than 0.01) in protein-deficient pigs in both experiments. Creatinine, total bilirubin, gamma-glutamyltransferase, alanine aminotransferase, and aspartate aminotransferase were elevated in protein-deficient pigs compared with controls after 7 weeks of depletion. Inorganic P (P less than 0.01), Ca (P less than 0.01), and Mg (P less than 0.05) concentrations were depressed in protein-depleted pigs compared with controls in both experiments. After 8 weeks of repletion in Experiment 1, all elements except inorganic P were similar in the two groups. Short-term, severe, protein malnutrition affected lipid, electrolyte, and structural mineral metabolism and indices of liver function in the absence of parasites, diarrhea, and infection. The effects were reversed after 8 weeks of repletion. We conclude that the elevated serum cholesterol in protein deficiency is related primarily to an increase in the HDL fraction.
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PMID:Response of blood serum constituents to production of and recovery from a kwashiorkor-like syndrome in the young pig. 135 73

We report the development of severe hepatotoxicity in a patient on zidovudine therapy who received 3.3 g of acetaminophen in less than 36 hours. Three days later, the patient's serum aspartate aminotransferase level was 5,724 U/L, alanine aminotransferase was 3,124 U/L, lactate dehydrogenase was 12,675 U/L, alkaline phosphatase was 84 U/L, and total bilirubin was 20 mumol/L. These values substantially improved over the ensuing 4 days. Serologic results for hepatitis B, hepatitis A, and cytomegalovirus were all negative. The pattern and time sequence of transaminase elevation in this patient are consistent with acute acetaminophen hepatotoxicity, especially since zidovudine-induced hepatotoxicity is described as producing cholestasis rather than acute hepatitis. We hypothesize that our patient's susceptibility to acetaminophen-dependent hepatotoxicity may have been augmented by competitive utilization of glucuronidation by other drugs such as zidovudine and/or trimethoprim-sulfamethoxazole with subsequent increased cytochrome P450-dependent metabolism of acetaminophen. Additionally, due to malnutrition and/or to human immunodeficiency virus infection per se, our patient may have had decreased hepatic reserves of glutathione with which to conjugate the toxic acetaminophen product of the P450 system. Although severe acetaminophen-associated hepatotoxicity has not previously been reported in patients receiving zidovudine, we suggest that clinicians be aware of this potential interaction and counsel malnourished patients, especially those with concomitant hepatic disease, to exercise caution when taking both these medications.
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PMID:Severe hepatotoxicity in a patient receiving both acetaminophen and zidovudine. 836 34

We examined total cholesterolemia, triglyceridemia, high density lipoproteins- (HDL) cholesterolemia, apolipoproteins A1 and B, body mass index, albuminemia and alanine aminotransferase in 60 heroin addicts. After comparing 23 control subjects with the heroin addicts the result was that the latter have significantly lower mean values of total cholesterolemia and of HDL-cholesterolemia and higher values of triglyceridemia. They also have significantly higher prevalences of cases of hypocholesterolemia and of hypo-HDL-cholesterolemia. Within the addict group there is no linear correlation between total cholesterolemia and body mass index; there is, however, an inverse linear correlation between total cholesterolemia and alanine aminotransferase. Therefore, the alterations found in the lipid pattern of heroin addicts are not due to malnutrition but hypothetically to liver diseases which are frequent in these patients.
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PMID:Plasma cholesterol and triglycerides in heroin addicts. 179 28

The authors describe two cases of Vit B1 and B6 deficiency in alcoholics with malnutrition. In the first case serum levels of AST and ALT, initially below norm became higher after Vit B1 and Vit B6 intake; the second, with AST and ALT above norm in previous months, had AST and ALT with normal activity during the disease. The authors suggest that normal activity of AST and ALT during alcoholic hepatopathy could be related to a depletion of Vit B1 and Vit B6.
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PMID:[Alcoholic hepatopathy, deficiency pathology and serum transaminases. Presentation of 2 clinical cases]. 192 89

Liver and biliary abnormalities are well-known complications of inflammatory bowel disease (IBD). It has been suggested that using total parenteral nutrition (TPN) may further impair liver function in these patients; this seems not to be so with total enteral nutrition (TEN). However, prospective trials comparing the incidence of liver function test (LFT) abnormalities with either TPN or TEN have not been carried out. Twenty-nine IBD inpatients with normal LFT, randomized to receive either TEN with a polymeric diet or isocaloric, isonitrogenous "all-in-one" TPN because of protein-energy malnutrition and/or severe disease, were included in the study. Sixteen patients (five with ulcerative colitis and 11 with Crohn's disease) received TEN, and 13 patients (eight ulcerative colitis and five Crohn's disease) were on TPN. All patients were on systemic steroids, and nine of them were on oral metronidazole. Both groups were homogeneous regarding age, sex, diagnosis, disease activity, nutritional status, daily nutrient supply, and days on artificial nutrition. Serum albumin levels significantly increased with TEN (32 +/- 1 to 38.2 +/- 1.6 g/liter, p less than 0.01), but not with TPN (32.1 +/- 2.2 to 33.9 +/- 1.4 g/liter, NS). Clinical improvement occurred in both groups of patients as shown by the change in the disease activity indexes. In all cases, measurements of serum alkaline phosphatase, serum bilirubin, aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyltransferase were performed weekly. There were no significant differences in the initial LFT between both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Liver function tests abnormalities in patients with inflammatory bowel disease receiving artificial nutrition: a prospective randomized study of total enteral nutrition vs total parenteral nutrition. 212 46


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