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)

Liver function tests include biochemical parameters (AST, ALT, GGT or Alkaline phosphatase), bilirubin and albumin levels and coagulation tests as prothrombin activity. These tests are commonly used in the routine screening even in symptomatic as in asymptomatic patients, and the right evaluation of the results is of vital importance. Cytolytic elevation in serum aminotransferases: In mild chronic elevation pharmacological toxicity, viral hepatitis, alcoholic and non-alcoholic fatty liver disease and hemochromatosis, should be excluded. Cholestatic elevation os serum enzymes: The first option should be to establish the origin of the alkaline phosphatase elevation, with the evaluation of the GGT levels to confirm the hepatic origin. The next step should be to distinguish the presence of an extrahepatic (biliary obstruction) or intrahepatic (PBC, PSC, drugs, etc) cholestasis, in these cases the most important test should be the abdominal ultrasound, in order to evaluate the biliary system. Hyperbilirubinemia: Non conjugated hyperbilirubinemia (hemolysis, ineffective erythropoiesis, Gilbert or Criggler-Najjar syndromes) and conjugated hyperbilirubinemia, an unusual situation in which Rotor and Dubin-Johnson Syndromes should be considered. The evaluation of albumin and prothrombin levels evaluates the hepatic function per se, allowing to differentiate between acute and chronic diseases. At present, there are not prospective studies to evaluate the efficacy of the liver function tests. To carry out a complete medical history, an appropriate physical examination and the appropriate application of non-invasive diagnostic tests (serology, iron levels, autoimmunity or abdominal ultrasound) allow to perform a right diagnosis in most patients, making more complex tests, including liver biopsy, secondary.
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PMID:[Utility of analytical parameters in the diagnosis of liver disease]. 1737 60

Evidence-based management guidelines for non-alcoholic fatty liver disease (NAFLD) are lacking in the Asia-Pacific region or elsewhere. This review reports the results of a systematic literature search and expert opinions. The Asia-Pacific Working Party on NAFLD (APWP-NAFLD) has generated practical recommendations on management of NAFLD in this region. NAFLD should be suspected when there are metabolic risk factors and/or characteristic changes on hepatic ultrasonography. Diagnosis by ultrasonography, assessment of liver function and complications, exclusion of other liver diseases and screening for metabolic syndrome comprise initial assessment. Liver biopsy should be considered when there is diagnostic uncertainty, for patients at risk of advanced fibrosis, for those enrolled in clinical trials and at laparoscopy for another purpose. Lifestyle measures such as dietary restrictions and increased physical activity (aerobic exercise) should be encouraged, although the best management strategy to achieve this has yet to be defined. Complications of metabolic syndrome should be screened for regularly. Use of statins to treat hypercholesterolemia is safe and recommended; frequent alanine aminotransferase (ALT) monitoring is not required. Obese patients who do not respond to lifestyle measures should be referred to centers specializing in obesity management; consideration should be given to bariatric surgery or gastric ballooning. The role of pharmacotherapy remains investigational and is not recommended for routine clinical practice. Non-alcoholic fatty liver disease should be recognized as part of the metabolic syndrome and managed in a multidisciplinary approach that addresses liver disease in the context of risk factors for diabetes and premature cardiovascular disease. Lifestyle changes are the first line and mainstay of management.
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PMID:How should we manage patients with non-alcoholic fatty liver disease in 2007? 1756 32

This study was designed to determine whether dietary epigallocatechin-3-gallate (EGCG), the most abundant catechin polyphenol in green tea, can protect the liver from cytochrome P450 2E1 (CYP2E1)-dependent alcoholic liver damage. Compared with an ethanol group, when EGCG was present in the ethanol diet, the formation of a fatty liver was significantly reduced and the serum aspartate transaminase (AST) and alanine transaminase (ALT) levels were much lower. Ethanol treatment significantly elevated hepatic CYP2E1 expression while simultaneously reducing hepatic phospho-acetyl CoA carboxylase (p-ACC) and carnitine palmitoyl-transferase 1 (CPT-1) levels. While EGCG markedly reversed the effect of ethanol on hepatic p-ACC and CPT-1 levels, it had no effect on the ethanol-induced elevation in CYP2E1 expression. EGCG prevents ethanol-induced hepatotoxicity and inhibits the development of a fatty liver. These effects were associated with improvements in p-ACC and CPT-1 levels. The use of EGCG might be useful in treating patients with an alcoholic fatty liver.
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PMID:Effect of dietary epigallocatechin-3-gallate on cytochrome P450 2E1-dependent alcoholic liver damage: enhancement of fatty acid oxidation. 1807 Dec 71

The correlation between biochemistry, imaging-studies and histology is a matter of controversy in non-alcoholic fatty liver disease (NAFLD) and the major pathophysiology of non-alcoholic steatohepatitis (NASH) is still unknown. We aimed to perform a comparative analysis between clinical, biochemical and histological variables of NAFLD. One-hundred and five NAFLD patients (F/M: 51/54), were studied, all with no-alcohol intake. The groups were followed-up for six months. Necroinflammation and fibrosis were more severe in patients with diabetes (p = 0.002, and p = 0.0001, respectively). In comparing NAFL to NASH, plasma nitric-oxide and malondialdehyde levels were significantly higher (p = 0.05, for-both), and vitamin-E and-C levels were significantly lower in NASH (p = 0.002, and 0.001, respectively). The serum ferritin levels were higher in NASH patients (p = 0.016). While the ultrasonographic grade was significantly higher, the liver-spleen density gradient was significantly lower in NASH group (p = 0.017, and 0.005, respectively). Within a six month period, serum ALT levels dropped into the normal range in 23/76 (30.3%) patients and serum ALT in the 6th month correlated significantly with the severity of steatosis, inflammation and fibrosis in initial biopsy (p = 0.023, 0.035, 0.011, respectively). In conclusion, the probability of severe liver disease is higher in patients with elevated-ALT in NAFLD. Serum ferritin levels have some prognostic significance in liver damage and fibrosis. Overt diabetes is predictive of advanced fibrosis and inflammation. However impaired glucose-tolerance is not. The advice on diet and exercise for six months after diagnosis may be a good strategy in NAFLD. The patients with normal-ALT without hepatomegaly, morbid-obesity and diabetes seem to have a good prognosis, however some of these patients may still require liver biopsy.
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PMID:Clinical, biochemical and histological correlations in a group of non-drinker subjects with non-alcoholic fatty liver disease. 1807 37

Evidence suggesting an effect of fetal growth on liver development and function stems from both animal and human studies. The association of birthweight with adult markers of liver damage and function was examined in a random sample of 2101 British women aged 60-79 years. Age-adjusted natural logged levels of alanine aminotransferase (ALT) and gamma glutamyltransferase (GGT) decreased linearly across increasing thirds of birthweight. Alkaline phosphatase (ALP) levels were higher in women of the lowest third of the birthweight distribution compared with other women. No evidence was found for associations of birthweight with aspartate aminotransferase (AST), total bilirubin and albumin. After full adjustment for social class, physical activity, smoking and alcohol consumption, an increase in one standard deviation of birthweight (691 g) was associated with a 2% ([95% CI 0%, 4%], P = 0.021) decrease in the geometric mean of ALT, a 4% decrease in GGT ([95% CI 1%, 6%], P = 0.008) and a 2% decrease in ALP ([95% CI 0%, 3%], P = 0.001). Associations of birthweight with ALT and GGT, but not with ALP, were attenuated when adjusting for components of the metabolic syndrome. These findings suggest that factors affecting intrauterine growth may increase the propensity for adult liver damage. The attenuation of associations with adjustment for components of the metabolic syndrome is in line with non-alcoholic fatty liver disease, indicated by elevated ALT and GGT, being the hepatic manifestation of the metabolic syndrome, and of the influence of perinatal factors on this syndrome.
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PMID:The associations between birthweight and adult markers of liver damage and function. 1817 79

Ezetimibe is a novel cholesterol and plant sterol absorption inhibitor that reduces plasma low-density lipoprotein-cholesterol by selectively binding to the intestinal cholesterol transporter, Niemann-Pick C1-Like 1. Mice deficient in Niemann-Pick C1-Like 1 are protected from high fat/cholesterol diet-induced fatty liver as well as hypercholesterolemia. The object of the present study was to determine whether ezetimibe treatment could reduce hepatic steatosis in diet-induced obese mice. C57BL/6J mice were fed a high fat/cholesterol containing semi-purified diet (45% Kcal fat and 0.12% cholesterol) for 7 months after weaning. These mice were not only obese, but also developed hepatomegaly and hepatic steatosis, with varying degrees of liver fibrosis and steatohepatitis. About 87% of the mice on the high fat/cholesterol diet for 7 months had elevated plasma alanine aminotransferase activity, a biomarker for non-alcoholic fatty liver disease. Chronic administration of ezetimibe for 4 weeks significantly reduced hepatomegaly by decreasing hepatic triglyceride, cholesteryl ester and free cholesterol in diet-induced obese mice fed high fat/cholesterol diet for 7 months. Chronic ezetimibe treatment also significantly decreased plasma alanine aminotransferase activity. These results suggest that ezetimibe may be a novel treatment for high fat/cholesterol-induced non-alcoholic fatty liver disease.
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PMID:Ezetimibe improves high fat and cholesterol diet-induced non-alcoholic fatty liver disease in mice. 1832 14

Oxidative stress is implicated in the pathogenesis of liver disease. We investigated oxidative stress-related parameters and correlated with clinical findings in 35 non-alcoholic fatty liver disease (NAFLD) patients, 38 alcoholic liver disease (ALD) patients and 38 normal subjects. NAFLD patients showed significantly higher body mass index, cholesterol, LDL-cholesterol, VLDL-cholesterol levels and transaminase activities compared to the other two groups. Haematological parameters were significantly altered in ALD patients and were reported only in male subjects. Glutathione content, catalase activity, glutathione reductase activity and glutathione peroxidase activity in NAFLD patients were reduced by 10.7 %, 18.5 %, 8.1 % and 16.8 %, respectively, and in ALD patients by 21.8 %, 29.6 %, 24.3 % and 45.3 %, respectively, compared to the normal group. However, thiobarbituric acid reactive substance content, superoxide dismutase activity and glutathione s-transferase activity were increased by 35.2 %, 31.6 % and 5.4 %, respectively, in NAFLD patients, and in ALD patients by 75.2 %, 72.7 % and 32.4 %, respectively, compared to the normal group. Oxidative stress is associated with collagen production and leads to fibrosis. Type IV collagen level in NAFLD patients (190.6 +/- 83 ng/mL) was significantly higher than in the normal group (124.5 +/- 14.5 ng/mL) and lower than in ALD patients (373.4 +/- 170 ng/mL). While type IV collagen level of >124 ng/mL was a predictor of NAFLD patients from normal subjects, elevated ALT (>40 IU/L) activity could discriminate either of the liver disease patients from normal subjects.
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PMID:Evaluation of blood oxidative stress-related parameters in alcoholic liver disease and non-alcoholic fatty liver disease. 1860 67

Fatty liver is one of the local morphological manifestations of metabolic syndrome and is frequently associated with insulin resistance. Insulin resistance is also common in patients with chronic hepatitis C. Hyperinsulinemia is an independent risk factor for hypertension and cardiovascular mortality. The aim of this study was to evaluate the therapeutic efficacy of angiotensin II receptor blockers (ARBs), telmisartan and olmesartan, for patients with non-alcoholic fatty liver disease (NAFLD) and chronic hepatitis C (CH-C). We analyzed the incidence of obesity, insulin resistance, and other disorders in patients with NAFLD (Group A), CH-C (Group B), or other liver diseases (Group C). We evaluated whether the ARBs, telmisartan and olmesartan, improved insulin resistance and liver injury by measuring the homeostasis model assessment ratio of insulin resistance (HOMA-IR) and serum alanine aminotransferase (ALT). The incidence of obesity (BMI > or =25 kg/m2) was significantly higher in Group A than in Groups B and C. The incidence of insulin resistance (HOMA-IR > or =2.5) in Groups A and B was significantly higher than in Group C. Regular doses of telmisartan and olmesartan significantly improved HOMA-IR and ALT levels not only in NAFLD patients but also in patients with CH-C. The effects tended to be more notable with telmisartan. In conclusion, telmisartan and olmesartan improved insulin sensitivity and may possibly be used as liver protecting agents in CH-C as well as NAFLD patients.
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PMID:Therapeutic effect of ARBs on insulin resistance and liver injury in patients with NAFLD and chronic hepatitis C: a pilot study. 1881 60

We examined the effect of heat-killed Lactobacillus brevis (L. brevis) SBC8803 on the development of alcoholic liver disease using ethanol-containing diet-fed mice. Heat-killed L. brevis was orally administered at a dose of 100 or 500 mg/kg once a day for 35 days. Alcoholic liver injury was examined by measuring the activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in a serum, and the alcoholic fatty liver was assessed from the content of triglyceride (TG) and total cholesterol in the liver. Quantitative RT-PCR was used to examine mRNA expression of tumor necrosis factor (TNF)-alpha, sterol regulatory element-binding protein (SREBP)-1, SREBP-2, and peroxisome proliferator-activated receptor alpha (PPARalpha) in the liver, as well as E-cadherin, Zonula occludens 1 (ZO-1), and heat shock protein (Hsp) 25 in the small intestine. Oral administration of L. brevis significantly inhibited an increase in the level of serum ALT and AST, as well as the content of TG and total cholesterol in the liver caused by ethanol intake. L. brevis supplementation suppressed the overexpression of TNF-alpha, SREBP-1, and SREBP-2 mRNA in the liver induced by ethanol intake and up-regulated the expression of Hsp25 mRNA in the small intestine. These results suggest that L. brevis ameliorated the ethanol-induced liver injury and the fatty liver by suppressing the up-regulation of TNF-alpha and SREBPs in the liver. We speculate that the inhibition of TNF-alpha and SREBPs up-regulation by L. brevis is due to the inhibition of gut-derived endotoxin migration into the liver through the enhancement of intestinal barrier function by the induction of cytoprotective Hsps.
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PMID:Oral administration of heat-killed Lactobacillus brevis SBC8803 ameliorates alcoholic liver disease in ethanol-containing diet-fed C57BL/6N mice. 1897 29

Determination of the liver histological lesions with noninvasive tests is an important part of the diagnostic work-up of patients with non-alcoholic fatty liver disease (NAFLD). We aimed to determine the predictive value of noninvasive biochemical markers, serum prolidase enzyme activity (SPEA), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and AST/ALT ratio for the liver histological lesions. Fifty-four liver biopsy-proven patients with NAFLD and 37 healthy controls were enrolled to the study. The diagnostic accuracies of biochemical markers were evaluated by receiver operating characteristic (ROC) curves and multiple linear regression analysis to predict the degree of fatty infiltration, lobular inflammation, NAFLD activity score, and stage of fibrosis. The SPEA of patients with steatohepatitis is significantly increased compared with the patients with simple steatosis and controls (1,338 [1,138-1,624] U/l; 974 [768-1,160] U/l; 972 [862-1,122] U/l, shown as median [25th-75th interquartile range], respectively, P < 0.0001). SPEA was positively correlated with the grade of liver fatty infiltration, lobular inflammation and NAFLD activity score, and stage of fibrosis, (r = 0.377, P < 0.005; r = 0.443, P < 0.001; r = 0.457, P < 0.001; r = 0.321, P < 0.018, respectively). SPEA was the best predictor for distinguishing steatohepatitis from simple steatosis according to the ROC analysis (area under the curve [AUC]: 0.85). Multivariate analysis revealed that the most useful single test for predicting lobular inflammation, NAFLD activity score, and fibrosis was SPEA, and for predicting the fatty infiltration, it was ALT (P < 0.00001, P < 0.001, P < 0.0001, P < 0.0001, respectively). This study demonstrated that SPEA can accurately predict the degree and stage of all histological lesions in NAFLD. It could be helpful for distinguishing steatohepatitis from simple steatosis and reducing the need for liver biopsy in the majority of patients with NAFLD.
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PMID:Diagnostic value of serum prolidase enzyme activity to predict the liver histological lesions in non-alcoholic fatty liver disease: a surrogate marker to distinguish steatohepatitis from simple steatosis. 1898 77


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