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)

Possible risk factors associated with mortality were studied in a community using data derived from annual mass health examinations for the aged mandated by law. A total of 1,804 adults (685 men and 1,119 women) aged 40 or older in A-town, located on Tsushima Island, Nagasaki Prefecture, Japan who had participated in annual health examinations at least once between 1984 and 1990, were followed for a mean period of 4.9 years. After adjustment for age using Cox proportional hazards models, in men liver dysfunction (aspartate aminotransferase > 40 U/l or alanine aminotransferase > 35 U/l), fasting blood glucose > or = 110 mg/dl and glucosuria, and in women serum creatinine > or = 1.2 mg/dl, fasting blood glucose > or = 110 mg/dl and proteinuria were found to be associated with a significantly increased risk of total mortality. In multivariate analysis using all independent variables that were significantly associated with mortality in age-adjusted bivariate analysis, in men liver dysfunction and hyperglycemia, and in women hypercreatininemia and hyperglycemia, were significant predictors of mortality. These independent variables remained significant or marginally significant predictors of total mortality even after excluding the effects of 3 pancreatic cancer cases with liver dysfunction or hyperglycemia or 12 deaths within the first year of follow-up, being associated with at least two-fold increased hazard rate ratios. From these results, it is recommended that persons with these risk factors be followed intensively and counseled by public health personnel to modify risk factors.
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PMID:[Results of annual health examination for the aged provided by the law that are predictive of increased mortality risk]. 787 66

The pathogenetic mechanism underlying glucose intolerance in pancreatic cancer is still unclear. We studied the pattern of three glucose regulating hormones (C-peptide, glucagon and GH) in pancreatic cancer patients with (N = 34) and without (N = 8) hyperglycemia, and compared the findings made with those from subjects with other hyperglycemic conditions of well-known origin [type I diabetes mellitus (8 cases) and diabetes mellitus secondary to chronic pancreatitis (13 cases) or liver cirrhosis (4 cases)]. In hyperglycemic pancreatic cancer patients, C-peptide was absent in 26% of the cases, reduced in 24%, elevated in 29% and within the normal range in the remaining 21%. In normoglycemic pancreatic cancer this hormone was reduced in two cases (25%) and within the normal range in all the others. GH was within the normal range in all cases: glucagon was below the normal range in some hyperglycemic pancreatic cancer patients (41%) or within the normal range in all the remaining patients. No correlations were found between the three hormones when findings from subjects were considered all together. However, in pancreatic cancer C-peptide and glucagon presented consensual variations. C-peptide, glucagon and GH levels were not related to tumor volume; glucagon was found to be associated with liver metastases. C-peptide was correlated with serum ALT and ALP. We may conclude that hyperglycemia associated with pancreatic cancer may be caused by different mechanisms. In some cases a reduced secretion of both insulin and glucagon was observed, as occurs in chronic pancreatitis. In the majority of patients, beta cell function appears normal, and the hyperglycemic state may depend on an altered peripheral sensitivity to insulin due to the pancreatic pathology itself or to consensual liver involvement.
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PMID:C-peptide pattern in patients with pancreatic cancer. 813 97

Plasma creatine phosphokinase, lactic dehydrogenase, glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase activities significantly increased in rats immersed in 23 degrees C water for 6 hr after restraint (water immersion stress). The stress-induced rises in the four enzymes were significantly prevented by the intraperitoneal injection of 6-hydroxydopamine (80 mg/kg), propranolol (1 and 10 mg/kg) or timolol (1 and 10 mg/kg) but not by phentolamine (0.1-10 mg/kg) and atropine (0.1-10 mg/kg). The stress also significantly increased plasma urea nitrogen and glucose levels; however, neither propranolol (0.1-10 mg/kg) nor timolol (0.1-10 mg/kg) did affect these levels. On the other hand, 6-hydroxydopamine (80 mg/kg) and phentolamine (10 mg/kg) slightly but significantly prevented the increase in plasma urea nitrogen level, and the stress-induced hyperglycemia was significantly prevented by either phentolamine (10 mg/kg) or atropine (1 and 10 mg/kg). Plasma norepinephrine and epinephrine levels were also increased significantly by the stress, and the norepinephrine response was suppressed significantly by 6-hydroxydopamine. In conclusion, excessive peripheral sympathetic activity possibly plays an important role in the water immersion stress-induced increases in the plasma enzymes activity primarily via beta-adrenoceptors, whereas alpha-adrenoceptors and the cholinergic nerves might be involved in the stress-induced increases in plasma urea nitrogen and glucose levels.
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PMID:Stress increases plasma enzyme activity in rats: differential effects of adrenergic and cholinergic blockades. 906 16

Intravenous injection into the rat of sublethal doses of Tityus serrulatus scorpion venom (100 micrograms protein/kg) or its major neurotoxin tityustoxin-I (TsTX-I, 20 micrograms/kg) caused, 30-180 min after injection, statistically significant increases in the serum levels of aspartate aminotransferase, amylase, creatine kinase and lactate dehydrogenase, as well as hyperglycemia, a high level of plasma free fatty acids and a low level of liver glycogen. The in vitro serum levels of the above enzymes did not change. For alanine aminotransferase, gamma-glutamyl transferase and alkaline phosphatase, neither in vitro nor in vivo alterations were observed. The whole venom and TsTX-I caused hepatic congestion with hemolysis and hydropic degeneration. Other histological lesions included edema and congestion with subpleural hemorrhage in the lungs, hypertrophy of fibers with degeneration areas in the heart, and congestion and hemorrhage in the kidneys. In the salivary glands, alterations to the acini and ductules were visible. In the adrenal glands no morphological alterations could be detected at the studied doses. The results suggest that the in vivo enzymatic and histopathological alterations are due to tissue lesions evoked by the whole venom and TsTX-I. An indirect effect, however, induced by stimulation of acetylcholine and catecholamine release in the postganglionic nerve terminals, cannot be excluded.
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PMID:Biochemical and histopathological alterations induced in rats by Tityus serrulatus scorpion venom and its major neurotoxin tityustoxin-I. 924 4

Alcohol intake per Japanese adult has been increasing year by year. To show biological effects of drinking, the dose-response relationships between alcohol use and serum indices were analyzed in 5919 Japanese men aged 40-59 years. The subjects were classified into nine groups: a nondrinking (ND, n = 1827) group and eight drinking (1D-8D) groups, by self-reported drinking habit. The 1D (the lightest drinking, n = 699), 5D (n = 942), and 8D (the heaviest drinking, n = 46) groups consumed alcohol less than 30 g per week, 25-30 g alcohol per day, and 100 g alcohol per day or more, respectively. Ten serum indices, total cholesterol, HDL cholesterol, triglyceride, total/HDL cholesterol ratio, LDL cholesterol, gamma-glutamyl transpeptidase, aspartate aminotransferase, alanine aminotransferase, glucose, and uric acid, were used. The dose-response analysis was statistically controlled for age, body mass index, smoking, and habitual exercise, and showed that drinking, even a small amount of alcohol, always had both beneficial and adverse effects on humans. However, alcohol less than 30 g per day may be tolerable for middle-aged Japanese men, because it improved serum lipids profile but did not induce apparent liver cell damage, hyperglycemia, or hyperuricemia.
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PMID:Dose-response relationships between drinking and serum tests in Japanese men aged 40-59 years. 1006 81

Urinalysis was carried out in 231 inpatients with alcohol dependence syndrome (215 males and 16 females). Fifty-nine patients (25.5%) showed proteinuria, 97 (42.0%) showed glucosuria, and 62 patients (26.8%) showed hematuria on admission. A total of 135 out of 231 patients (58.4%) showed abnormal urinalysis. Proteinuria was related to high blood pressure, high serum glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, lactate dehydrogenase, uric acid, and triglyceride levels, and high urinary amylase concentration. Glucosuria was related to high serum glutamic-oxaloacetic transaminase concentration and a history of gastrectomy. Hematuria was related to high age and high urinary amylase levels. By chi-square test, there was a significant correlation between proteinuria and hematuria (p < 0.001) and between hematuria and glucosuria (p < 0.001), but no correlation was found between proteinuria and glucosuria. The incidence of diabetes mellitus was 10.8% (25 out of 231 patients), but transient hyperglycemia was observed in some patients without diabetes mellitus on admission. Elevated hemoglobin A1, hemoglobin A1c, and fructosamine concentrations were observed in patients with either impaired glucose tolerance or transient hyperglycemia, which suggested the presence of persistent hyperglycemia before admission. On discharge, only 12 out of 198 patients (6.1%) showed abnormal urinalysis. We report that heavy ethanol consumption induces transient abnormal urinalysis results in Japanese alcoholics.
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PMID:Induction of transient proteinuria, hematuria, and glucosuria by ethanol consumption in Japanese alcoholics. 1039 97

In this work we investigate the possible toxicity of vanadyl sulfate (VOSO4), a compound capable of reducing hyperglycemia, on the following serum enzymes of diabetic young rats: alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LD) and creatine kinase (CK), as well as its effects on serum lipids. We find that at a concentration of 1 mg/mL VOSO4 has no toxic effect on the liver and muscles of diabetics young rats. These findings suggest that VOSO4 may be an alternative to insulin in the near future, due to its low cost, low toxicity and ready availability.
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PMID:Effect of oral vanadyl sulfate treatment on serum enzymes and lipids of streptozotocin-diabetic young rats. 1049 91

Prolonged hyperglycemia inhibits B-cell function by mechanisms that are largely unclarified. We investigated the involvement of advanced glycation end products (AGEs), using aminoguanidine as well as the AGE-breaking compound ALT-711 in a transplantation model. Islets from Wistar-Furth rats were transplanted under the kidney capsule of syngeneic streptozocin-diabetic recipients. Aminoguanidine was administered as 1 g/L in the drinking water. Graft-bearing kidneys were isolated and perfused to investigate insulin secretion, and grafts were excised to measure preproinsulin mRNA contents. In all transplants to diabetic rats, insulin responses to 27.8 mM glucose were abolished and aminoguanidine failed to correct this abnormality. However, aminoguanidine treatment for 8 weeks following transplantation increased preproinsulin mRNA contents of the grafts (P < 0.05). In addition, treatment with aminoguanidine enhanced the insulin secretory response to arginine (P < 0.05). Arginine-induced insulin secretion was also enhanced when aminoguanidine treatment was started after an initial 2-week implantation period rather than immediately after transplantation. On the other hand, treatment with ALT-711 (0.1 mg/kg by gavage) for 8 weeks completely failed to affect B-cell function of grafts, and ALT-711 was also ineffective under in vitro conditions. Our findings indicate that aminoguanidine effects in vivo are to a major extent not coupled to AGEs or nitric oxide synthetase inhibition, but possibly to oxidative modifications accomplished by the guanidine compound.
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PMID:Improvement by aminoguanidine of insulin secretion from pancreatic islets grafted to syngeneic diabetic rats. 1082 71

Having developed a non-insulin-dependent diabetes mellitus (NIDDM) syndrome model in the rabbit using Wirsung duct ligation, it appeared interesting to use it to study the relationship between glycemia and the plasma levels of TXA(2)and PGI(2), and of some other biochemical parameters such as cholesterol, triglycerides, alkaline phosphatase and transaminases. A comparative study was carried out in the sham-operated rabbits (controls, C) and those having their pancreatic duct ligatured (NIDDM, D) at 15, 30, 40, 50 and 60 days post-ligation. On the 40th days, whereas in the controls, glycemia was 1.17 +/- 0.04 g.l(-1), it reached a maximum of 4.62 +/- 0.76 g.l(-1)(25.40 mM) in the NIDDMs. No significant modification was observed either in cholesterolemia or in triglyceridemia in either group. The GOT and GPT were highly increased, from 11.50 +/- 4.00 IU. l(-1)and 27.00 +/- 1.50 IU.l(-1)(C) to 37.50 +/- 5.64 IU.l(-1)(P<0. 001) and 58.50 +/- 7.50 IU.l(-1)(D) (P<0.001) in the NIDDM group, suggesting that hyperglycemia occurred simultaneously with the degeneration of the pancreatic tissue. In parallel, in D rabbits, the plasma levels of TXB(2)and 6 keto PGF(1alpha)were augmented to 68.22 +/- 6.20 pg.ml(-1)versus 22.49 +/- 5.74 pg.ml(-1)(C) (P<0.001), and 127.11 +/- 14.39 pg.ml(-1)versus 48.65 +/- 4.51 pg.ml(-1)(C) (P<0. 001) respectively. Statistical studies showed a significant correlation (P<0.05 and <0.02) between glycemia and the biosynthesis of eicosanoids under study. Moreover, 25 mM was found to be the threshold level of glucose excess essential to increase the TXA(2)and PGI(2)biosynthesis significantly. This supports the results obtained by other authors studying the action of glucose on phospholipase activity and consequent eicosanoid production.
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PMID:Modifications in the TXA(2) and PGI(2) plasma levels and some other biochemical parameters during the initiation and development of non-insulin-dependent diabetes mellitus (NIDDM) syndrome in the rabbit. 1088 59

Hyperlipidemia is a known risk factor for fatty infiltration of the liver, a condition that can progress to cirrhosis and liver failure. The objectives of this study were to document the prevalence of fatty infiltration in the livers of hyperlipidemic patients and to identify the predictor variables associated with this condition. Over an 18-month recruitment period, clinical, biochemical, and radiologic assessments were performed in a cross-sectional manner in 95 adult patients referred to an urban hospital-based lipid clinic for evaluation and management of hyperlipidemia. The mean (+/-SD) age of the patients was 55 +/- 13 years. Forty-eight (51%) were male. Fifty-two patients (55%) had hypercholesterolemia, 25 (26%) severe hypertriglyceridemia, 14 (15%) mixed hyperlipidemia, and 4 (4%) moderate hypertriglyceridemia. Obesity and diabetes were present in 36 (38%) and 12 (12%) of cases, respectively. A total of 61 (64%) patients had elevated liver enzyme tests. The most common enzyme abnormalities were an elevated serum ALT in 45 (47%) and GGT in 43 (45%) of patients. Ultrasound findings revealed diffuse fatty liver in 47 patients (50%), of which 21 cases (22%) were mild, 18 (19%) moderate, and 8 (9%) severe. The majority of patients with hypercholesterolemia [35/52 (67%)] had normal ultrasounds, whereas severe hypertriglyceridemia and mixed hyperlipidemia were frequently associated with radiologic evidence of fatty liver (odds ratios 5.9 and 5.1 respectively, P < 0.01). Independent predictors of fatty liver were; AST (P = 0.001), hyperglycemia (P = 0.02), and age (P = 0.04). In a model incorporating known risk factors for fatty liver, diabetes was the only risk factor other than hypertriglyceridemia that was significantly associated with fatty infiltration. No such effect was seen with age, gender, obesity, or alcohol consumption. In conclusions, the results of this study indicate that ultrasonographic evidence of fatty infiltration of the liver is evident in approximately 50% of patients with hyperlipidemia. Hypertriglyceridemia is the lipid profile most often associated with this condition. Serum AST values, hyperglycemia, and age independently predict the presence of fatty infiltration, while hypertriglyceridemia and diabetes are the only risk factors that significantly increase the risk of fatty infiltration in hyperlipidemic patients.
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PMID:Fatty infiltration of liver in hyperlipidemic patients. 1111 62


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