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)

The therapeutic effectiveness of nutritional support in the treatment of severe chronic hepatitis and posthepatitic cirrhosis was evaluated. 143 patients with severe chronic hepatitis and 83 with posthepatitic cirrhosis were evaluated with SGA for assessing the nutritional status before the treatment. Patients with severe chronic hepatitis were divided into three groups: group A subject to enteral nutrition (EN) and parenteral nutrition (PN), group B subject to comprehensive treatment (CT)+PN; group C subject to CT+EN. The patients with posthepatitic cirrhosis were divided into two groups: group D receiving CT and group E receiving CT+PN+EN. The function of liver and kidney and nutritional status were monitored to assess the therapy in 6 weeks. The results showed before treatment, over 90 % patients had moderate to severe malnutrition. After nutritional support, the liver function (ALT, T-bil) and nutritional status (TP, TC) in group A was improved significantly as compared with that in groups B and C (P<0.05). Compared with group D, the values of TP and Alb were increased significantly in group E (P<0.05), but the levels of ALT, AST and T-bil had no obvious change. It was suggested that most patients with severe chronic hepatitis or posthepatitic cirrhosis had malnutrition to varying degrees. The nutritional support treatment could obviously improve the nutritional status of these patients, and was helpful to ameliorate the liver function of the patients with severe chronic hepatitis. Among the methods of nutritional support treatment, PN combined with EN had the best effectiveness.
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PMID:Nutritional support treatment for severe chronic hepatitis and posthepatitic cirrhosis. 1685 Jul 51

Choline is an essential nutrient; dietary deficiency of choline is associated with impaired liver function, elevated blood concentrations of alanine aminotransferase, creatinine phosphokinase and homocysteine. There is also depletion of acetylcholine concentration in the brain, leading to deficit in memory function. The authors examined the dietary intake of choline in groups of students at the Mona Campus of the University of the West Indies. Sixty-two medical students (first and second years) and biochemistry students (final year) were recruited They were asked to (including amounts) record all foods and drinks consumed for three days (two weekdays and one weekend day). The sheets were collected and the amount of choline and betaine (a metabolite of choline) consumed were calculated Dietary intake of folate was also evaluated. The analysis revealed that 86.2% of the females and 90.9% of the males reported diets that delivered less daily choline than the adequate intake quoted by the Institute of Medicine of the National Academy of Sciences, USA (425-550 mg/day). The betaine consumption ranged between 25 to 620 mg/day (no adequate intake documented) and the folate consumed was more than the recommended daily allowance of folate (180-200 microg/day). The dietary intake of choline in the majority of students is below adequate intake. Although folate also serves similar functions to choline, it is unlikely that it can substitute for choline in all physiological aspects and therefore the implications of low dietary choline need further investigation.
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PMID:Choline: are our university students eating enough? 1708 6

The alcoholic liver disease usually causes overall immunological alterations which might be attributed to hepatic disease, to ethanol action, and/or to malnourishment. In the present study, efficacy of lecithin with vitamin-B complex to treat ethanol induced immunomodulatory activity was compared with the effect of lecithin alone and tocopheryl acetate (vitamin E). Ethanol (1.6 g/kg body wt/day for 12 weeks) exposure increased thiobarbituric acid reactive substance (TBARS) level, while decreased superoxide dismutase (SOD) activity and reduced glutathione (GSH) content in whole blood hemolysate of 8-10 week-old male BALB/c mice (weighing 20-30 g). The activities of transaminase (AST and ALT) enzymes, interleukin (IL)-10 and gamma interferon (IFN-gamma) elevated, while IL-2 and IL-4 reduced in mice serum due to ethanol exposure. These suggested that oxidative stress and immunomodulatory activities were interdependent and associated with ethanol induced liver damage. Lecithin treatment significantly reduced AST (32.44%), ALT (32.09%), IL-10 (25.63%) activities and TBARS content (12.76%) compared to ethanol treated group. However, lecithin with vitamin-B complex treatment, significantly reduced AST (62.83%); ALT (61.96%); IL-10 (35.88%); IFN-gamma (22.55%) activities and TBARS content (31.58%), while significantly elevated GSH content (36.49%) and SOD activity (61.21%). Tocopheryl acetate treatment significantly reduced AST (62.83%); ALT (61.54%); IL-10 (36.35%): IFN-gamma (23.28%) activities and TBARS content (35.84%). while significantly elevated GSH content (28.76%) and SOD activity (62.42%) compared to ethanol treated group. These findings persuasively argued that lecithin with vitamin-B complex was a new promising therapeutic approach in controlling ethanol induced immunomodulatory activities involving liver damage processes. Prevention of oxidative stress with correction of nutritional deficiency caused alteration in the ethanol-induced immunomodulatory activities and associated liver diseases.
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PMID:Effect of lecithin with vitamin-B complex and tocopheryl acetate on long-term effect of ethanol induced immunomodulatory activities. 1787 44

Deficiency in plasminogen activator inhibitor-1 (PAI-1) gene expression is known to promote growth factor activation and regeneration in a number of hepatotoxicity models. To evaluate if PAI-1 has similar effects in acetaminophen (APAP) hepatotoxicity, wild-type (WT) and PAI-1 gene knockout mice (PAI-KO) were treated with 200 mg/kg APAP and liver injury and its repair were assessed. In WT animals, plasma alanine aminotransferase (ALT) activities increased during the first 12 h and then returned to baseline within 48 h. The area of necrosis increased in parallel to the ALT values, peaked between 12 and 24 h and was completely resolved by 96 h. The regenerative response of cells outside the necrotic area, as indicated by proliferating cell nuclear antigen protein and cyclin D(1) gene expression, was observed within 24 h, peaked at 48 h and then declined but remained elevated until 96 h. Liver injury in response to APAP was similar in PAI-KO as in WT animals during the first 12 h. However, plasma ALT values and the area of necrosis further increased during the following 12 h with development of massive intrahepatic hemorrhage. Approximately, 50% of the PAI-KO animals did not survive. Although liver injury of the surviving animals was repaired, the regeneration process was delayed until 48 h. A potential reason for this delay may have been due to the more severe injury and/or the increased expression of the cell cycle inhibitor p21. Our data indicate that PAI activation limits liver injury and mortality during APAP hepatotoxicity by preventing excessive hemorrhage and thereby facilitating tissue repair.
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PMID:Plasminogen activator inhibitor-1 limits liver injury and facilitates regeneration after acetaminophen overdose. 1846 30

Acute ingestion of acetaminophen can induce a dose-dependent hepatotoxicity and lead to death. The management of acute acetaminophen poisoning at the early stage is well codified. A reported amount of ingestion > 200 mg/kg in a child, > 150 mg/kg in an adult (125 mg/kg if risk factors are present) require hospitalisation. Activated charcoal is administered within 1-2 hours of ingestion. AST/ALT levels are measured on admission, 12 hours after, and according to outcome every 12-24 h. N-acetylcysteine (NAC) administration within 8-10 hours protects against acetaminophen-induced hepatotoxicity. The two protocols of NAC administration, intravenous and oral, have a comparable effectiveness. NAC is indicated if the serum acetaminophen level drawn 4 hours after ingestion and plotted on the nomograme falls above the "200 mg/L-4 hours" line. Nomograme is not usable with repeated acute ingestion or repeated supratherapeutic doses; presence of risk factors (enzymatic induction, malnutrition, chronic alcoholism) must be taken into account ("100 mg/L - 4 hours" line). Outcome is favorable with respect to these conditions.
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PMID:[Acute acetaminophen overdose]. 1863 Aug 24

Patients with Inflammatory Bowel Disease (IBD) are exposed to nutritional risk. Malnutrition in Crohn's Disease (CD) and to a somewhat lesser in Ulcerative Colitis (UC) is very frequent. Depending on the severity of the disease, weight loss has been reported in 65% to 76% of those with CD and in 18% to 62% of those with UC. The role of Total Parenteral Nutrition (TPN) is essential in very severe cases where enteral nutrition is not tolerated or standard drug therapy is not effective. Nutritional therapy is important for the correction of nutritional deficiency, especially in cases where elective surgical treatment is required. This study examined the effects of preoperative TPN administration in patients with IBD. Since 1990, 29 pts, 13 (44.8%) male and 16 (55.2%) female with severe IBD; 16 (55.2%) with UC and 13 (44.8%) with CD were treated with TPN in our department in the preoperative period. Evaluation of this group was compared with a group which was not treated with TPN preoperatively: 61 pts, 34 (55.7%) male, 27 (44.3%) female; 50 (82%) with CD, 11 (18%) with UC. Evaluation of this group was compared with the group of patients who were subjected to surgical procedure without prior TPN administration, in total a number of 61, of whom 34 (55.7%) were male and 27 (44.3%) female patients. In this group, the number of patients with CD and UC was 50 (82%) and 11(18%) respectively. During the course of the study, the following parameters were examined: Body mass index (BMI), Disease Activity Index (CDAI/AI), laboratory parameters and the number of hospital days. The parameters were analysed before the surgical intervention, and one week and six months after the surgical intervention. The duration of the application of TPN was 12.5 +/- 5 days. The analysis of these parameters has shown that there is no statistically significant difference in the number of hospital days in both groups, which was 18.9 +/- 8.9 in the intervention group and 18.9 +/- 6.5 days in the control group, p = 0.9808, but analysis of the Disease Activity (CDAI/AI) has shown that patients who were on TPN were in a more severe stage of the disease. In the TPN treated group of patients none, 0 pts (0%), of the pts had no Index of Activity, 1.7 pts (24.1%) had Index 2 and 22 (75.9%) had Index 3. In the other group 3 pts (4.9%) had Index 1; 39 pts (63.9%) had Index 2 and 19 pts (31.2%) had Index of Activity 3. During the monitoring period of six months the activity of the disease was lower in patients treated with TPN. The BMI in the group of patients treated with TPN was lower in both sexes. It was lower than 18.4 in 7 males and 5 females; between 18.4 and 19.9 in 2 males and 4 females; between 19.9 and 25 in 3 males and 6 females; between 25 and 19.9 in 1 male and 1 female; there were no pts with BMI higher than 29.9. In the control non-TPN group, 5 males and 3 females had BMI < or = 18.4; 2 males and 5 females had between 18.4 and 19.9; 23 males and 13 females had between 19.9 and 25; 3 males and 5 females had between 25 and 29.9 and 1 male and 1 female had BMI higher than 29.9. The BMI had an increasing trend in the postoperative period in both groups. The laboratory parameters that we examined were: number of erythrocytes and sedimentation, number of leukocytes, haemoglobin levels, total number of lymphocytes, albumin level, C-reactive protein, orosomucoid, electrolytes; sodium, potassium, calcium and serum iron, the enzymes (AP, AST and ALT); level of bilirubin and urea and creatinine. The results were analysed using the Tukey honest significant difference test (HSD), ANOVA and Student t-test. Statistically significant differences were observed between preoperative and postoperative period in both groups. The intergroup comparison showed significant differences in the level of albumin, AST, ALT and bilirubin.
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PMID:Total parenteral nutrition in treatment of patients with inflammatory bowel disease. 1870 98

This study comprehensively describes the effects of various levels of food reduction on a wide range of toxicological parameters in dietary-optimized rats (fed with approximately 75% of ad libitum food consumption daily; 16 g and 22 g/day for females and males, respectively) that has been established as a nutritionally appropriate and well-controlled animal model in conducting toxicity studies. Toxicological parameters, including general condition, ophthalmology, clinical pathology and anatomic pathology, were examined in dietary-optimized Crl:CD(SD) female and male rats fed 16 g and 22 g/day (control), 12 g and 17 g/day (75% group), 8 g and 11 g/day (50% group), or 4 g and 6 g/day (25% group), respectively for 2 weeks. There was mortality and morbidity including reddish urine in 25% group females. The reddish urine was identified as "hemoglobinuria" that resulted from extra/intra-vascular hemolysis induced by severe food reduction. Hemoconcentration, decreased leukocytes and platelets, decreases in nutritional elements (serum glucose, protein, and lipids), increased aspartate aminotransferase and alanine aminotransferase, imbalanced electrolytes, and/or decreased urinary pH were observed in all restriction groups. Histopathologically remarkable changes included erythrophagocytosis in the spleen/liver and renal tubular necrosis with hyaline cast/droplets in 25% group; in addition to bone marrow depletion, lymphoid depletion in thymus/spleen/lymph node, and/or decreased secretion in the prostate/seminal vesicle in all restriction groups. Most of these changes were considered attributable to nutritional deficiency, dehydration, accelerated protein catabolism, stress and/or hemolysis secondary to severe food reduction. These results will enable toxicologists to help distinguish primary drug-induced effects from secondary changes associated with decreases in food consumption.
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PMID:Effects of reduced food intake on toxicity study parameters in rats. 1904 75

We have reported previously that dietary medium-chain triacylglycerol (MCT) improved serum albumin concentration and protein balance in malnourished rats. To clarify the mechanisms for this effect of MCT, hepatic messenger RNA levels of gluconeogenic enzymes, pyruvate dehydrogenase (PDH) and alanine aminotransferase (ALT) were measured in rats fed low-protein diets containing either MCT or isocaloric long-chain triacylglycerol (LCT) for 2 wk. The serum albumin concentration in rats fed the MCT diet was significantly higher compared with those fed the LCT diet. Serum free fatty acids and ketone body fraction were higher in rats fed MCT compared with those fed the LCT diet. The hepatic mRNA level of PDH was significantly lower in rats fed MCT than those fed LCT. But, there was no significant difference between the two groups in mRNA of gluconeogenic enzymes or ALT. These results suggest that ketone bodies, which are an alternative energy source and might spare blood glucose, increase by MCT feeding, and the reason for the PEM (protein-energy malnutrition)-improving effect of MCT is not caused by suppression of gluconeogenesis.
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PMID:Effects of dietary medium-chain triacylglycerol on mRNA level of gluconeogenic enzymes in malnourished rats. 1915 91

Protein-energy malnutrition and inflammation are among the leading causes of poor outcome in hemodialysis patients. Hepatitis C virus (HCV) infection is accompanied by elevated proinflammatory mediators, also found in dialysis patients with malnutrition-inflammation complex syndrome. We aimed to study the rate and characteristics of malnutrition-inflammation complex syndrome (MICS) in hemodialysis patients, especially those with hepatitis C. The study included 147 patients (mean age 55.1 +/- 12.9 years), 24.5% of whom were HCV-positive, undergoing adequate hemodialysis three times a week for the last 52.7 +/- 52.5 months. Parameters of nutrition and inflammation were investigated to evaluate MICS. HCV-positive vs. HCV-negative patients had significantly higher hematocrit (29.6 +/- 4.5 g/dL vs. 28.1 +/- 4.3, P < 0.05), uric acid (345.8 +/- 96.5 vs. 321.3 +/- 118.8 micromol/mL, P < 0.05), aspartate aminotransferase (AST, also known as serum glutamic oxaloacetic transaminase [SGOT]) (23.3 +/- 14.9 vs. 17.8 +/- 9 U/L, P < 0.008), alanine aminotransferase (ALT, also known as serum glutamic pyruvic transaminase [SGPT]) (41.2 +/- 28.7 vs. 26.6 +/- 17.1 U/L, P < 0.0003), serum creatinine (980.4 +/- 219.1 vs. 888.4 +/- 202.9 micromol/mL, P < 0.022), intact parathyroid hormone (329.7 +/- 630.5 vs. 110.2 +/- 145.3 pg/mL, P < 0.002), malnutrition-inflammation score (7.4 +/- 5.2 vs. 5.6 +/- 4.1, P < 0.038), and Charlson comorbidity index (4.5 +/- 1.5 vs. 4 +/- 1.4, P < 0.05). MICS had a prevalence of 20-40% in our study. HCV-positive patients had a significantly higher prevalence of MICS than HCV-negative patients (30-40% vs. 20-30%).
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PMID:Malnutrition-inflammation complex syndrome and hepatitis C in maintenance hemodialysis patients. 1937 50

Ethanol metabolism promotes the formation of a variety of reactive aldehydes in the liver. These aldehydes can rapidly form covalent protein adducts. Accumulating evidence indicates that these protein adducts may contribute to ethanol-mediated liver injury. Overproduction of gamma-ketoaldehydes, levuglandins (LGs) and isolevuglandins, is implicated in the pathogenesis of several chronic inflammatory diseases. gamma-Ketoaldehydes can form protein adducts orders of magnitude more quickly than 4-hydroxynonenal (4-HNE) or malondialdehyde. We hypothesized that ethanol-induced oxidative stress in vivo results in overproduction of LGE(2)- and iso[4]LGE(2)-protein adducts in mouse liver. Female C57BL/6 mice were allowed free access to an ethanol-containing diet for up to 39 days or pair-fed control diets. Pathological markers of ethanol-induced hepatic injury including serum alanine aminotransferase, hepatic triglyceride, and CYP2E1 were elevated in response to ethanol feeding. Ethanol-induced formation of iso[4]LGE(2)-, LGE(2)-, and 4-HNE-protein adducts in mouse liver was dependent on both dose and duration of ethanol feeding. Deficiency of cyclooxygenase 1 or 2 did not prevent ethanol-induced iso[4]LGE(2) or LGE(2) adducts in the liver, but adduct formation was reduced in both TNFR1- and CYP2E1-deficient mice. In summary, ethanol feeding enhanced gamma-ketoaldehyde-protein adduct production via a TNFR1/CYP2E1-dependent, but cyclooxygenase-independent, mechanism in mouse liver.
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PMID:Formation of gamma-ketoaldehyde-protein adducts during ethanol-induced liver injury in mice. 1961 18


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