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

A community health survey of 923 residents aged 30 years or more was performed in Putai Township of Taiwan. To elucidate the relationships between hepatitis C virus (HCV) and surrogate tests for non-A, non-B hepatitis in hyperendemic areas of hepatitis B virus (HBV) serum levels of alanine aminotransferase (ALT), triglycerides, cholesterol, hepatitis B surface antigen (HBsAg) and antibody to HCV (anti-HCV) were examined. Glucose tolerance tests and the history of diabetes treatment were used to define the diabetes status. Fatty liver was diagnosed by sonography. The prevalence of anti-HCV was 2.6% (95% confidence interval, 1.6-3.6%). Elevated ALT and fatty liver were significantly associated with anti-HCV in univariate analysis. Anti-HCV was not an associated factor for fatty liver after adjusting for serum triglycerides and cholesterol, sex, body mass index and diabetes status through multiple logistic regression. However elevated ALT was still associated with anti-HCV after adjusting for serum triglycerides, sex, body mass index, HBsAg and age through multiple linear regression. The anti-HCV prevalence was similar between HBsAg-positive and negative subjects. Aggregation of HCV infection was found among spouses. It was concluded that elevated ALT and intimate contact with HCV carriers might be associated factors for HCV infection, and that HBV infection and fatty liver were not related to HCV infection in Taiwan.
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PMID:Relationship between fatty liver, alanine aminotransferase, HBsAg and hepatitis C virus. 138 55

Although it has been reported that vanadate is effective in diminishing the expression of diabetes in the rat, the severe toxic side effects noted in the vanadate-treated animals suggest that chronic oral administration of vanadate argues against its use in human diabetes. The present study was conducted to evaluate the effects of the chelator Tiron on the mobilization of vanadium after administration of sodium metavanadate in the drinking water (0.20 mg/ml) of streptozotocin-induced diabetic rats for 35 days. Intraperitoneal treatment with Tiron (300 or 600 mg/kg) was initiated after three weeks of vanadate administration and continued for two weeks. The ameliorative effects of vanadium with respect to diabetes were not diminished by the administration of Tiron, but the accumulation of vanadium in kidney and bone was significantly decreased in the Tiron-treated groups and diabetes associated increases in serum GOT, GPT and cholesterol were diminished with Tiron treatment. It is concluded that the coadministration of metavanadate and Tiron may be of potential value for treatment of diabetes mellitus.
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PMID:Tiron administration minimizes the toxicity of vanadate but not its insulin mimetic properties in diabetic rats. 153 46

The poor survival rate of patients with extrahepatic bile duct tumors is well documented. Over the course of 4 years, we treated a white woman with diabetes diagnosed with histologically proven adenocarcinoma of the common bile duct with six injections of dihematoporphyrin ether followed by seven photodynamic therapy treatments to the biliary duct. As of July 1989, the patient was still alive, was not jaundiced, and had a Karnofsky performance status of 70. No changes occurred in any blood chemistry value from the time of injection to the time of photodynamic therapy. Of the transient elevations of some blood chemistry values and the white blood cell count, which occurred within 24 to 48 hours after photodynamic therapy, only those of alanine aminotransferase, aspartate aminotransferase, and amylase were significant.
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PMID:Photodynamic therapy to treat tumors of the extrahepatic biliary ducts. A case report. 182 76

It has been generally accepted that congestive heart failure does not lead to fulminant hepatic failure, unless it is associated with cardiac shock or low cardiac output. Only three cases have been reported, in which liver congestion is followed by fulminant hepatic failure without a history of shock or low cardiac output. Here we present a case of a 48-year-old man with dilated cardiomyopathy and pulmonary infarction, who developed fulminant hepatic failure from congestion. When he was admitted for the control of diabetes mellitus, hepatomegaly of 3-finger breadth and marked cardiomegaly without pulmonary congestion was noted. Diabetes was controlled using insulin. But 3 weeks after admission, he sometimes complained of back dullness because of pulmonary infarction. His heart gradually increased in size, and Jugular venous dilatation and pretibial pitting edema also worsened. Jaundice was noted and serum GOT and GPT increased. A large liver of 6-finger breath below the right costal margin was able to be felt. But within one week, the size of the liver markedly decreased and the signs of hepatic failure such as jaundice, hepatic encephalopathy and numerous petechiae appeared. Blood pressure was maintained and no hypotension or cardiac shock was noted. The patient died of fulminant hepatic failure on the 20th days after onset of the hepatic failure. The autopsy revealed liver atrophy with severe central lobular necrosis, and thrombus in the right main pulmonary artery which caused severe pulmonary infarction. The mechanism of fulminant hepatic failure not accompanied with low cardiac output is discussed.
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PMID:[A case of fulminant hepatic failure secondary to congestive heart failure]. 187 44

To determine the therapeutic effect of the carinitine palmitoyltransferase I (CPT-I) inhibitor, etomoxir, eight hospitalized obese non-insulin-dependent diabetes mellitus (NIDDM) patients were studied (body mass index [BMI], 28.7 +/- 1.3 kg/m2; age, 54 +/- 8 years [means +/- SE]) at baseline (placebo = t1), and after oral etomoxir (50 mg/d = t2, 100 mg = 3, 150 mg = t4, 200 mg = t5, placebo = t6). Fasting blood glucose (mmol/L), triglycerides (mmol/L), cholesterol (mmol/L), free fatty acids (mumol/L), beta-hydroxybutyrate (mumol/L), and alanine aminotransferase (GPT, U/L) were determined (t1 to t6), as were glucose utilization (M value; indirect calorimetry) and hepatic glucose production during a 10 mU/kg.min euglycemic clamp (t1 and t4). A dose-dependent decrease was induced by etomoxir in fasting blood glucose (t1 to t5: 9.5 +/- 0.7, 8.7 +/- 1.0, 8.3 +/- 1.1 [P v t1 less than .05], 7.8 +/- 0.9, [P v t1 less than .01], 7.9 +/- 1.1 [P v t1 less than .05]), which was reversible in t6 (9.9 +/- 1.1). Mean plasma lipids were reduced (t1 v t5) for triglycerides (-54%, P v t1 less than .01), cholesterol (-24%, P v t1 less than .05), and beta-hydroxybutyrate (-44%, P v t2 less than .01), while free fatty acids increased by 52% (P v t1 less than .05), as did GPT (t1: 17 +/- 3; t5: 32 +/- 7 U/L [P v t1 less than .01]).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition by etomoxir of carnitine palmitoyltransferase I reduces hepatic glucose production and plasma lipids in non-insulin-dependent diabetes mellitus. 194 47

Aspartate aminotransferase, alanine aminotransferase and gamma-glutamyl transferase activities were measured in sera from 411 diabetic outpatients and were raised in 26 (6.4%), 34 (8.3%) and 62 (15.2%) patients, respectively. Serum total bile acid concentrations were raised in 4 patients (1%). Percentage glycated hemoglobin A1, serum fructosamine concentration and plasma glucose concentration were also measured. No relationship between the presence of raised enzyme activity and mature age, short duration of diabetic treatment regimen or glycemic control was found. Twenty-six patients with an alanine aminotransferase activity greater than 60 U/l were reviewed at 23 +/- 6.5 weeks. The activity of this enzyme had fallen to within the reference interval in 15 (58%). In the other 11 patients, its median activity was 75 U/l (range 51-181 U/l). Median gamma-glutamyl transferase activity had risen in these 11 patients from 78 U/l to 93 U/l (P less than 0.01). No statistical differences in treatment regimen or glycemic control were found between these two groups. Raised liver-associated enzyme activity in treated stabilised diabetic outpatients should therefore not be attributed to poor glycemic control or diabetic treatment regimen.
Diabetes Res Clin Pract
PMID:Raised liver associated enzyme activity and post-prandial bile acid concentrations in sera from treated diabetic outpatients. 197 26

The purpose of our study was to determine if streptozotocin induced diabetes (SID) in rats produces alterations in hepatic function, as described in poorly controlled diabetic patients, and if islet transplantation (islet-Tx) would subsequently ameliorate this status. Hepatocellular dysfunction was evaluated by the aspartate aminotransferase (SGOT) and the alanine aminotransferase (SGPT) activities in plasma. For the evaluation of cholestasis the plasma alkaline phosphatase (APase) activity was used. These determinations were performed in normal, SID, SID with Islet-Tx, and SID Wistar rats with sham-Tx. Also, glucose was measured in plasma samples, as well as histological studies of the liver were performed. More than 1,000 isogeneic islets (islet-Tx group) or non viable insular tissue (sham-Tx group) were transplanted via mesenteric ileal vein three weeks after SID. The results showed that SID in rats produces alterations in the hepatic function as well as in the structure of the hepatocytes, and the normalization of carbohydrate metabolism by islet transplantation restores normal hepatic function and morphology.
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PMID:Normalization of the altered liver function tests after islet transplantation in diabetic rats. 226 34

In 1214 adult persons, the relationship between alcohol consumption, the "liver enzymes" and other metabolic parameters, including the serum lipids, were investigated. In 798 of the persons, glucose tolerance tests with measurement of plasma insulin were performed (young and old male and female adults, either volunteers or patients without liver-related diseases). There was a high correlation of the three transferases GOT, GPT and GGT not only with the reported alcohol consumption but also with the plasma insulin. Most of the insulin increase, however, occurred in that range of the three transferases which, so far, has erroneously been considered to be the normal one. The C-peptide showed the same behaviour. Plasma insulin was also raised in relation to overweight, but only in persons with the sum of the three transferases over 30 U/l, not in persons who did not drink alcohol and who had really normal transferases (sum of the three transferases below 30 U/l measured at 25 degrees C). The quotient of plasma insulin divided by the relative body weight (Broca Index) was constantly low in the range of really normal transferases (up to 30 U/l), thereafter rising significantly, but only in the range of the transferases so far erroneously considered to be the normal one (GOT to 17, GPT to 22, GGT to 28 U/l, thus sum up to 67). Serum glucose in the tolerance test also rose with the transferases but much less than the plasma insulin. The correlation between both GGT and the sum of the three transferases with the plasma insulin was significantly positive and independent of the relative body weight. It is concluded that overweight (which is generally believed to be the main risk factor for non-insulin-dependent diabetes), and insulin resistance (which leads to hyperinsulinaemia), are largely caused by the toxic effects of "normal" daily alcohol, more in the human male than in the female. Hyperinsulinaemia (which blocks lipolysis) is caused by a toxic effect of ethanol and its metabolites, independent of caloric input and overweight. Hyperinsulinaemia is at least in the human male at present, probably the most important cause of obesity. In obesity, caused by "normal" alcohol consumption, a vicious circle occurs: the enhancement of the triglycerides and, consequently, the free fatty acids leads to a further decrease of glucose utilization by the muscle. A continuously high glucose level has toxic effects: eventually the beta cells of the pancreas are exhausted.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The main cause of diabetes (type II): "normal" alcohol drinking]. 227 72


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