Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Current belief that vitamin B6 deficiency causes depletion of muscle phosphorylase in animals appears to be erroneous. We present evidence that vitamin B6 deficiency is ineffective in reducing total phosphorylase in gasttocnemius muscle of young rats over a period of at least 8 weeks. Rats that had accumulated high levels of muscle phosphorylase while ingesting diets containing normal or excess amounts of the vitamin retained their phosphorylase after transfer to a vitamin B6 deficient diet. Prolonged deficiency did ultimately lead to enzyme depletion but this was after anorexia had developed and weight loss had occurred. When rats were partially starved for 1 to 4 days (fed 10% of normal energy intake) they lost muscle phosphorylase while retaining alanine and aspartate aminotransferases. When totally starved, the rats lost more phosphorylase than during partial starvation, but completely retained alanine aminotransferase, and lost some aspartate aminotrasferase. We conclude that the behavior of muscle phosphorylase is consistent with the Krebs-Fischer proposal that it acts as a reservoir for vitamin B6 and that starvation, but not vitamin B6 deficiency per se, causes depletion of muscle phosphorylase. It appears that phosphorylase may function as an adjunct ot adipose tissue necessary for the animal to efficiently meet the exigencies of starvation.
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PMID:The behavior of muscle phosphorylase as a reservoir for vitamin B6 in the rat. 63 54

Adenylosuccinase activity of rat liver is depressed by prolonged starvation, cortisol administration, high protein diets, and alloxan diabetes. The loss of activity is not due to the accumulation of a dissociable inhibitor or loss of a cofactor. Starvation produces no loss in activity for 1 day; thereafter the activities of the liver and spleen enzyme decay with a half-life of about 0.9 day. Starvation produces no change in the activity of the kidney, brain, and skeletal muscle enzyme. Refeeding restores the activity of the liver enzyme to the fed level, with only a slight overshoot. The recovery of adenylosuccinase activity is equally rapid after refeeding a balanced diet, or corn oil, or glucose, and is not inhibited by injection of glucagon, in contrast to malic enzyme activity. Recovery is inhibited by cycloheximide, indicating the involvement of protein synthesis. Althouth adenylosuccinase is depressed in liver of starving rat it is elevated in liver of starving chicken. Starvation depresses malic enzyme activity and elevates alanine aminotransferase activity in both species. When rats are starved, the rate of de novo synthesis of adenine mononucleotide decreases in spleen and liver but not in kidney, suggesting a regulatory role for adenylosuccinase in purine biosynthesis. The low activity of adenylosuccinase in liver of severely starved rats is inconsistent with the proposal (Moss, K. M., and McGivan, J.D. (1975) Biochem. J. 150, 275-283) that the purine nucleotide cycle plays a major role in ammonia production for urea synthesis, at least under these conditions.
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PMID:Effect of diet on adenylosuccinase activity in various organs of rat and chicken. 69 Jan 30

L-Leucine-pyruvate transaminase (mol. wt. 70 000) in Gluconobactersuboxydans synthesized during nitrogen starvation contained a labile form which changed to the stable one later. The labile enzyme (mol. wt. 70 000) dissocated to the two proteinaceous components: a cationic one (mol. wt. 10 000--20 000) and an anionic one (mol. wt. 50 000--60 000), during column chromatography on DEAE-cellulose. The enzyme activity was reconstructed when they were mixed. The reconstructed enzyme had almost the same molecular size and enzymatic properties as the labile and the native stable enzymes.
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PMID:Resolution and complementation of the labile L-leucine-pyruvate transaminase. An intermediate during enzyme formation under nitrogen starvation in Gluconobacter suboxydans. 100 28

Coccinia indica (Family: Cucurbitaceae, locally known as telakucha) leaves were extracted with 95% ethanol. Following evaporation of the solvents, the residue was suspended in distilled water. When this suspension was fed orally to male normal-fed and 48-hr starved rats, the blood glucose was lowered 21% (P less than 0.01) in normal-fed and 24% (P less than 0.001) in 48-hr starved animals respectively. Starvation had induced a 3-fold increase in the activity of glucose-6-phosphatase and this activity was depressed 19% (P less than 0.05) by extract feeding while basal activity of the enzyme in normal-fed rats remained unaffected. Consistent with the depression of glucose-6-phosphatase, urea cycle enzyme arginase was also depressed 21% (P less than 0.001) and 12% (P less than 0.01) in the liver of 48 hr-starved and normal-fed animals respectively. Unlike glucose-6-phosphatase, starvation induced levels of gluconeogenic enzymes alanine aminotransferase and aspartate aminotransferase were not affected by Coccinia extract. These results suggest that the hypoglycemic effect of C. indica is partly due to the repression of the key gluconeogenic enzyme glucose-6-phosphatase.
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PMID:Hypoglycemic effects of Coccinia indica: inhibition of key gluconeogenic enzyme, glucose-6-phosphatase. 133 43

A total of 365 donor hepatectomies performed between May 1985 and March 1990 were reviewed and analyzed retrospectively to identify risk factors associated with poor graft function and to study the outcome of grafts retrieved from "marginal" donors. The donor mean age was 27.1 years (8-69 years). Mean ICU donor stay was 2.7 days (range 0 to 18 days), and the mean ischemic time was 8.6 hr (range 3 to 22 hr). The pancreas was retrieved in 39 donors. Donor's weight above 100 kg was the only variable found to be associated with both significantly increased 3-month graft loss (P less than 0.01) and early hepatocellular damage--AST or ALT greater than 2000 U/ml, 1st day posttransplant (P less than 0.02). Prolonged stay in the ICU (greater than 3 days), although associated with a significantly increased rate of hepatocellular damage (P less than 0.05), did not affect early graft survival. A systolic blood pressure less than 90 mmHg despite the use of high-dose dopamine (greater than 15 micrograms/mg/min), but not each of these variables itself, was also associated with a significantly increase rate of hepatocellular damage (P less than 0.001). All other variables, including age greater than 50, ischemic time greater than 12 hr, combined liver-pancreas procurement, and liver function test abnormalities, did not affect the outcome. We conclude that extending our limits to accept donors of the higher age group and those who have moderately abnormal liver function tests or a prolonged ischemic time will not jeopardize our results. It is suggested to perform liver biopsy in overweight donors during the retrieval to prevent using grafts with severe fatty infiltration. It is hypothesized that hormonal changes, starvation, and increased risk to develop infection might jeopardize the outcome of grafts from donors with a prolonged ICU stay. Although 70% of the early hepatocellular injuries are reversible, the remaining 30% result in graft failure.
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PMID:The use of marginal donors for liver transplantation. A retrospective study of 365 liver donors. 173 33

We reviewed retrospectively a cohort of 80 patients with hyperemesis gravidarum hospitalized between 1976 and 1986 for the presence of abnormal liver enzymes and ketonuria. Thirteen (16%) had abnormal liver enzymes, generally less than four times the upper limit of normal. In this group, hyperemesis gravidarum began at the 14th week of pregnancy as compared to the 6th week in the normal enzyme group (p less than 0.01). Both groups were similar with regard to age, number of children and pregnancies, and duration of vomiting. Ketonuria was significantly more severe (p less than 0.01) in the abnormal enzyme group, implying a more severe state of starvation and dehydration. The correlation coefficient between the degree of ketonuria and level of liver enzymes was low for alkaline phosphatase (r = 0.18), GPT (r = 0.15), and GOT (r = 0.28). The concept that dehydration and starvation are important factors for the induction of liver cell injury is supported by our data. Lack of correlation between the degree of ketonuria and liver enzyme levels is suggestive of other mechanisms (hormonal, genetic) that may interact to produce transaminasemia.
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PMID:Abnormal liver enzymes and ketonuria in hyperemesis gravidarum. A retrospective review of 80 patients. 236 99

The activities of alanine-, aspartate- and branched-chain amino-acid transaminases, glutamine synthetase, glutamate dehydrogenase and adenylate deaminase in white adipose tissue of adult male rats have been determined in animals submitted to 12-h cold exposure (4 degrees C) or to 24-h food deprivation. Starvation resulted in small changes in glutamate dehydrogenase and alanine transaminase when expressed per unit of protein weight, inducing an increase in branched-chain amino-acid transaminase and glutamine synthetase. Cold exposure showed the same effects as starvation with respect to glutamate dehydrogenase and alanine transaminase, but induced increases in glutamine synthetase and aspartate transaminase. It is concluded that starvation increases the handling of some amino acids by white adipose tissue and the detoxification of the ammonia thus evolved. The changes observed suggest a different pattern of amino-acid metabolism enzyme changes with either cold or starvation.
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PMID:Amino-acid metabolism enzyme activities in rat white adipose tissue. 243 May 32

Alkaline phosphatase (ALP, EC 3.1.3.1), acid phosphatase (ACP, EC 3.1.3.2), aspartate aminotransferase (ASAT, EC 2.6.1.1) and alanine aminotransferase (ALAT, EC 2.6.1.2) were measured in the mucosal homogenates of the duodenum, jejunum and caecum of full-fed (control), starved and refed White Rock Cockerels. Starvation caused a significant (p less than or equal to 0.05) increase in the activity of ACP in all three segments of the intestine. Subsequent re-feeding brought the activity back to the control level. In contrast ALP activity fell in the duodenum during starvation and was partially restored by refeeding. In the jejunum and caecum the ALP activity decreased during starvation and was fully restored by re-feeding only in the caecum. ASAT activity increased (p less than or equal to 0.05) during the entire period of starvation in all three segments. Re-feeding failed to decrease the enzyme activity within 48 hours. Starvation caused a reduction (p less than or equal to 0.05) in the activity of ALAT and re-feeding did not increase the activity in the duodenum and jejunum. The caecum showed no change in the activity during fasting.
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PMID:The activities of phosphatases and aminotransferases in the epithelium of the small intestine and caecum of white rock cockerels during starvation. 255 Nov 9

1. Adult, female Xenopus laevis were subjected to 12 months of starvation. 2. Starvation resulted in a continuous reduction in the activity of both hepatic and renal glucose-6-phosphate dehydrogenase. 3. Fructose-1,6-diphosphatase was significantly reduced at months 10 and 12 in the liver, and at months 4, 10, and 12 in the kidney. 4. Pyruvate kinase activity of muscle and liver decreased during the experimental period whereas the renal enzyme remained essentially unchanged. 5. Both hepatic and renal glutamate-pyruvate transaminase (GPT) and hepatic glutamate-oxaloacetate transaminase (GOT) showed a reduction of activity after 2 and 4 months of starvation followed by an increase in GPT but not in GOT.
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PMID:Long-term starvation in Xenopus laevis Daudin--III. Effects on enzymes in several tissues. 255 3

Sporidesmin, a hepatotoxin from Pithomyces chartarum, is responsible for facial eczema in ruminants. In an attempt to clarify the biochemical processes supporting sporidesmin toxicity and response of the liver, haematology, plasma biochemistry and liver enzyme changes were monitored for 21 days in a model for facial eczema resulting from a single intraperitoneal injection of 2.8 mg/kg BW sporidesmin to guinea pigs. Most plasma disturbances were observed 8 days after administration and accounted for starvation, liver cytolysis, and cholestasis or liver enzyme induction. Alterations of hepatic enzyme activities were intense with a maximum increase on days 2 for alkaline phosphatases (ALP) and 8 for gamma-glutamyltransferase (GGT), and a maximum decrease on day 21 for aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT). Comparison of liver and plasma enzyme changes indicates that GGT was the most reliable and significant plasma indicator of sporidesmin-associated liver alterations. Moreover, this study points out the validity of the one-dose intoxicated guinea-pig model for research on sporidesmin biochemical toxicity and pathobiology of facial eczema.
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PMID:Liver enzyme changes in a guinea-pig model of facial eczema (sporidesmiotoxicosis). 257 Jun 91


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