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)

In alloxan diabetes, serum GOT, GPT, and ceruloplasmin were significantly increased compared to normal rats, while the level of serum alkaline phosphatale was decreased. Treatment with insulin led to lowering of serum GOT, GPT, and ceruloplasmin while serum alkaline phosphatase remained low. Then lycanol or daonil were used for treatment, serum GOT, GPT, and ceruloplasmin were changes towards normalization, while ceruloplasmin returned to normal values. Serum-alkaline phosphatase increased after 7 and 14 days from treatment with oral hypolygylcaemic drugs. In dithizonized diabetic animals, the levels of serum GOT, GPT, and alkaline phosphatase were found to be higher than normal, while ceruloplasmin levels were unchanged. After treatment with insulin all serum enzyme activities were normalized.
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PMID:Serum enzyme changes in experimental diabetes before and after treatment with some hypoglycaemic drugs. 41 44

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

Gentamicin treatment caused an elevation in serum urea and creatinine concentrations and ALT activity, associated with pathological changes in the liver and kidney. The pathological and blood chemistry changes were more severe in diabetic gentamicin-treated than in non-diabetic gentamicin-treated rats. Alloxan-diabetic rats had lowered blood glutathione concentrations which may have been responsible for the enhancement of gentamicin toxicity in these rats.
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PMID:Comparison of gentamicin toxicity in normal and diabetic rats. 147 82

We measured aminotransferase activity and vitamin B6 content in the livers of diabetic mice. Two different types of mice were used for the measurements, spontaneously non-obese diabetic (NOD) or alloxan-induced diabetic (Allo) mice, and control mice were either non-diabetic NOD or Institute of Cancer Research (ICR). The liver of diabetic mice had more aspartate aminotransferase (AST) activity than those of normal mice. The diabetic livers also had more vitamin B6 than did normal livers, and pyridoxamine (PM) levels were particularly high but pyridoxal (PL) levels were not. ICR livers showed hepatic alanine aminotransferase activities inversely correlated with blood glucose concentrations, while diabetic livers did not. The abundance of AST and B6 in the diabetic liver is consistent with the great need for gluconeogenic substrate there. This is understandable in that most aminotransferases require B6 vitamins, and especially the correlation between s-AST and PM levels was recognized in the diabetic liver. Conversely, the AST and PM levels were negatively correlated in normal mice. A metabolic shift towards gluconeogenesis apparently produces more B6 and PM while it induced holo-AST synthesis.
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PMID:Changes on levels of B6 vitamin and aminotransferase in the liver of diabetic animals. 237 34

Enzyme activity in the livers of mice was studied in examining the metabolic disturbances of diabetes. Spontaneously non-obese diabetic (NOD) mice, mice with alloxan-induced diabetes (Allo), and control ICR mice were used. As NOD mice undergo a spontaneous pathogenic process over time, younger and older NOD mice were compared (non-diabetic and diabetic) as were control ICR mice. Two liver enzymes became more active with age, aspartate aminotransferase (AST) and alanine aminotransferase (ALT). AST activity increased more in the hyperglycemic mice, i.e., the diabetic NOD and the Allo mice, than in the normoglycemic group, i.e., the ICR and non-diabetic NOD mice. Abnormally high AST activity was seen in the cytosolic fraction of the liver but not in the mitochondrial fraction. The changes in enzyme activity in diabetic mice were independent of any age-associated changes. The higher AST levels in diabetic mice are thought to be consistent with their greater need for gluconeogenic substrate. AST showed a more notably higher increase than did ALT in this study, and lactate dehydrogenase showed no significant changes.
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PMID:Aminotransferase activity in the liver of diabetic mice. 340 35

Studies with brain alanine aminotransferase showed higher activity of the enzyme in the soluble fraction of cerebellum. Among the tissues, the liver soluble fraction was the richest source of the enzyme. Alloxan-induced diabetes caused both regional and time-dependent variations in the activity of brain alanine aminotransferase. Significant among these changes were the decrease in both soluble and particulate enzyme from cerebral hemispheres and an increase in the soluble enzyme activity from cerebellum at early stages of diabetes. Brain stem did not show any marked change in enzyme activity. Liver and heart enzyme, however, increased significantly after 1-2 weeks of diabetes. Insulin treatment to diabetic animals caused an 'over-shoot' in soluble alanine aminotransferase activity, particularly in cerebellum and liver.
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PMID:Influence of alloxan diabetes and insulin treatment on the activity of alanine aminotransferase in rat brain regions, liver and heart. 391 Apr 25

Biochemical changes in the placenta were studied using alloxan-induced diabetes mellitus in the female rat. In comparison with a control group (n = 13) the placentas of the diabetic animals (n = 12) had significantly higher glucose, glycogen and protein levels. It was, however, shown that this supply of substrate was inadequately utilised for energy, as ATP/ADP quotient was lower and the ADP content was significantly higher. Metabolism still appeared to take place under aerobic conditions, as evidenced by the unchanged lactate levels. In terms of the protein content of the placentas, the activity of the enzymes we investigated (GOT, GPT, LDH, G-6-PDH, MDH, ICDH) was lowered by 25-44%. These results support the idea of global placental insufficiency in diabetics.
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PMID:Effects of alloxan-induced diabetes mellitus on the metabolism of the rat placenta. 395 50

1. The concentrations of alanine, aspartate, glutamate, glutamine and serine plus threonine have been measured by enzymic methods in ;quick-frozen' livers from normal, starved, alloxan-diabetic and phlorrhizin-treated rats. 2. The hepatic concentrations of alanine and serine plus threonine were decreased in rats starved for 48hr. Treatment of these rats with phlorrhizin resulted in a rapid fall (within 2(1/2)hr.) in the concentrations of all the glucogenic amino acids except serine plus threonine, which increased. The pattern for alloxan-diabetic rats was similar to that for phlorrhizin-treated animals, except that here serine plus threonine also decreased in concentration. 3. The effects of anoxia on the hepatic concentrations of the glucogenic amino acids are reported. 4. Inhibition of glutamate-pyruvate transaminase in vivo by l-cycloserine resulted in the accumulation of alanine in situations involving high rates of gluconeogenesis from endogenous amino acids. 5. Measurements of the concentrations of the reactants of the glutamate-pyruvate transaminase and glutamate-oxoglutarate transaminase systems in various metabolic states suggest that they are both at or near equilibrium in rat liver. 6. New enzymic methods are described for the determination of serine plus threonine and alanine.
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PMID:Concentrations of free glucogenic amino acids in livers of rats subjected to various metabolic stresses. 604 91

Suspensions of isolated rat hepatocytes incubated in the presence of the diabetogenic agent alloxan exhibit time- and concentration-dependent damage. At concentrations of 3.5 mM and above, alloxan caused an increase in lactate dehydrogenase (LDH), glutamate-pyruvate transaminase (GPT) and intracellular potassium (K+) leakage, all of which are indices of plasma membrane damage, and decreased the intracellular reduced glutathione content (GSH) of the cells. Preincubation (10 min) in D-glucose (50 or 100 mM, but not 10 mM) partially protected the hepatocytes from LDH, GPT and K+ leakage and the decrease in GSH produced by alloxan (7 mM) during a 60-min incubation period. Other sugars (D-galactose, 2-deoxy-D-glucose, D-fructose, D-mannoheptulose and D-mannitol) were also found to protect hepatocytes against damage caused by alloxan. D-Fructose was found to be the most potent protective sugar. These results indicate that alloxan is not selectively toxic to the pancreatic beta-cell and that sugars can protect against alloxan-induced cytotoxicity in hepatocytes.
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PMID:Alloxan toxicity in isolated rat hepatocytes and protection by sugars. 715 55

The intravenous injection of zinc chloride immediately before and 15 minutes after alloxan or dithizone prevented the usual hyperglycaemia observed 24 hours after induction of diabetes. The intravenous injection of manganese chloride prevented any marked rise of blood glucose, while chromium and cobalt chlorides lowered the blood glucose level to a certain extent. In alloxan diabetic rats, serum GOT and GPT levels were significantly higher than normal. The serum GOT levels were higher in animals injected with chromium than cobalt, zinc and manganese; while serum GPT levels were higher in cobalt than in chromium, zinc and manganese. In dithizone diabetes, serum GOT and GPT were increased in animals injected with cobalt than chromium, zinc and manganese. Alloxan diabetic rats showed lower serum alkaline phosphatase levels and higher in animals injected with cobalt than chromium, zinc and manganese. For dithizone, there are statistically significant differences in all cases. In alloxan diabetes, coeruloplasmin was higher than normal, while intravenous injection of dithizone was without effect on serum coeruloplasmin.
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PMID:Serum enzyme changes due to trace amounts of some transition metal ions on the induction of experimental diabetes. 742 63


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