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)

1000 consecutive blood donors had their liver functions studied. 110 donors (11%) were found to have raised ALT of more than twice normal levels. 29 donors had liver biopsies done. Histologically 23 had fatty change, 5 had chronic persistent hepatitis and 1 had liver cirrhosis. Fourteen out of the 23 donors with fatty change also had hypercholesterolemia and hypertriglyceridemia. Viral serology of the 110 donors showed that 3 donors were HBsAg positive, 5 donors were Anti-HAV (IgM) positive and 20 donors were Anti-HBc (IgM) positive. Majority of donors with raised ALT had fatty liver on biopsy with only 6 donors having significant findings of chronic persistent hepatitis and cirrhosis. Serologically, most of the donors (74.5%) with raised ALT had no markers of Hepatitis A, Hepatitis B, CMV or EBV. An interesting finding is the high incidence (18%) of positive, Anti HBc (IgM) in donors with raised ALT.
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PMID:Liver disease in blood donors with raised transaminases. 375 95

Excessive fat accumulation in the liver is a common metabolic disorder seen in humans and animals. Fatty liver was induced in the rat by feeding the animals with a sucrose rich diet containing 1% orotic acid for 2-3 weeks. In the sera from fatty liver rats there were significant changes in the level of alanine aminotransferase (+ 68.7%), malic dehydrogenase (+ 77.8%), gamma-glutamyl transpeptidase (- 53.4%) and total lipids (+ 26.6%). There were small to no changes in the levels of aspartate aminotransferase, glucose-6-phosphate dehydrogenase, lactic dehydrogenase, aldolase, malic enzyme, 6-phosphogluconic acid dehydrogenase, alkaline phosphatase and albumin. In fatty liver, significant differences were seen in the levels of glucose 6-phosphate dehydrogenase (+ 235%), malic enzyme (+ 170%), gamma-glutamyl transpeptidase (+ 113%), 6-phosphogluconate dehydrogenase (+ 63%), aspartate aminotransferase (+ 35.6%), malic dehydrogenase (+ 38%), lactic dehydrogenase (+ 37%), and alanine aminotransferase (- 23%). Comparison of the non-fatty part with the fatty part of the fatty liver showed larger changes in the non-fatty part of the liver, suggesting that during the fattening process, there is an induction of enzymes in the liver reaching a peak prior to lipid accumulation, declining thereafter during liver fattening. The increase in NADPH-generating lipogenic enzymes suggests that accumulated fat in the liver is at least partially from de-novo increased synthesis in the liver.
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PMID:Biochemical changes in liver and blood during liver fattening in rats. 377 7

An experimental model for monitoring rat liver function during protracted exposure to hepatotoxic agents is proposed. Owing to their invasiveness, the models usually employed are appropriate for studying the mechanism of action of toxic substances, but do not allow the liver situation to be followed over the course of time. The need to sacrifice animals to determine liver triglycerides-one of the key parameters in the progress of toxic damage- reduces the possibility of following such progress in the same animals. This study describes the testing of a model for monitoring three basic parameters of liver injury: cytolysis, steatosis and metabolic deficiency of the liver. CCl4 has been chosen as model-hepatotoxin. Steatosis is determined by evaluating the triglyceride content of small specimens of liver, obtained through open-field biopsies, which appear to be representative of the whole liver. Fatty liver is paralleled by the block in Triton-induced hypertriglyceridaemia. Determination of serum triglycerides derives from a very poorly invasive technique which can be repeated several times. The combination of these tests with the assessment of both the cytolysis (ALT and SDH release into the circulation) and the impairment of the efficiency of liver microsomal enzymes (TMO clearance), seems to offer a reliable experimental procedure in predicting the hepatotoxic effect of xenobiotics.
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PMID:A model for monitoring changes in liver function. 379 13

The features on computed tomographic (CT) scans of nonalcoholic fatty liver were investigated in 24 patients with nonalcoholic fatty liver related to overweight. CT examinations were performed before and after 3 months of a low-calorie diet. The reversibility of fatty infiltration during diet therapy could be monitored by changes in appearance on repeated CT scans. Hepatic steatosis improved, as assessed from increases in attenuation values on CT scans after 3 months of the diet, and the improvement was accompanied by a decrease in the elevated serum glutamic-pyruvic transaminase activity. Hepatic fatty infiltration in these patients was not always uniform, and attenuation values in the right lobe of the liver were significantly lower than those in the left lobe. After the 3-month diet therapy, the mean liver volume was significantly reduced, while the spleen volume was unchanged. Two sequential CT examinations, performed before and after diet therapy, may be useful for evaluating obese patients with elevated serum transaminase activity.
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PMID:Obesity-related nonalcoholic fatty liver: CT features and follow-up studies after low-calorie diet. 380 3

The effect of nicardipine on experimental hyperlipemia induced by a 1% cholesterol diet in spontaneously hypertensive rats (SHR) was investigated by the change of hemodynamics and the determination of lipid contents of the serum, liver, heart and aorta. Nicardipine increased liver weight and liver weight per body weight ratio, and it decreased heart and kidney weight significantly. Nicardipine inhibited the increase in blood pressure with cholesterol and normal diets. Nicardipine decreased heart rate in SHR fed the normal diet, and it inhibited the increase in heart rate in SHR fed the cholesterol diet. Serum lipid levels significantly increased with the cholesterol diet. Nicardipine significantly increased cholesterol in high density lipoprotein (HDL-C) and phospholipid in HDL (HDL-PL) with cholesterol and normal diets, and it decreased triglyceride and improved the atherogenic index "(total cholesterol-HDL-C)/HDL-C" with the normal diet. Serum GOT and GPT significantly increased with the cholesterol diet. Nicardipine significantly enhanced an increase in GOT and GPT levels with the cholesterol diet. Nicardipine increased phospholipid content in the liver, triglyceride in the heart, and it decreased total cholesterol in the aorta. A morphologic study showed a fatty liver in SHR fed the cholesterol diet, but nicardipine had no effect on the morphological changes in the liver, heart and aorta. These results suggest that nicardipine may prevent atherosclerotic degeneration by the inhibition of hypertension, increase in serum HDL and decrease in total cholesterol in the aorta.
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PMID:[Effect of nicardipine on cholesterol-fed S.H.R]. 405 35

The effect of intestinal bacterial flora and endotoxin on fatty liver with germfree (GF) and conventional (CV) rat in the 12th and 24th week was investigated after giving fatty diet which was added 1% cholesterol-0.5% cholic acid to the basic diet. Results are as follows. Serum biochemistry Serum GOT, GPT, ALP and cholesterol values increased after giving the fatty diet in both groups. Limulus Gelation Test In CV group, endotoxin was detected in 2 of 10 cases in portal blood and was completely absent in arterial blood. After the fatty diet, endotoxin increased gradually both in portal and arterial blood. Cyclic AMP values on glucagon challenge (P/B ratio) In both groups, the levels of the P/B ratio maintained low values compared with control. In CV group, the values were lower in endotoxin positive cases than negative ones. Hepatic carbohydrate metabolism Abnormal hepatic F6P , glucose, FDP and PEP values were observed in CV group and reduction of the levels of hepatic F6P , G6P and glucose values were remarkable in GF group. Hepatic G6P in CV group and FDP in GF group remained unchanged. Impairment of F6P and G6P in CV group, was significant in endotoxin positive cases than in negative ones.
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PMID:[Pathogenesis of endogenous endotoxemia in chronic liver disease--with special reference to the experimental fatty liver in germfree animals]. 632 43

The role of dietary sucrose concentrations in the development of hepatic steatosis in rats was investigated. Twelve groups of weanling male Sprague-Dawley rats received semipurified diets with different sucrose concentrations ranging from 20 to 50% (w/w); one group received a cereal-based chow diet. Rats were sacrificed after 3 weeks and body weight, liver/body weight ratio, plasma alanine aminotransferase concentration, hepatic triglyceride concentration, and liver morphology (light and electron microscopy) were determined. Body weight and liver/body weight ratio were decreased in rats receiving 40-50 or 25-35% dietary sucrose compared to rats receiving 20% sucrose or chow. Plasma alanine aminotransferase concentrations were within normal limits. Hepatic triglyceride concentration was significantly increased in rats receiving 40-50 and 25-35% dietary sucrose compared to rats receiving 20% dietary sucrose or chow. Light microscopy showed hepatic steatosis in a periportal distribution at all concentrations of dietary sucrose. Both the frequency and the severity of the steatosis were increased with increasing dietary sucrose concentrations. Electron microscopy from selected livers with increased hepatic triglyceride concentrations revealed increased lipid spheres and increased smooth endoplasmic reticulum without prominent Golgi apparatus or GERL complex. It is concluded that high dietary sucrose concentrations are responsible for the development of hepatic steatosis. Semipurified diets with high dietary sucrose concentrations such as the AIN-76A diet (50% sucrose) should not be used in animal studies in which increased triglyceride deposition could influence experimental outcome.
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PMID:Hepatic steatosis in rats fed diets with varying concentrations of sucrose. 651 Jun 14

It has been reported that fatty liver is not uncommon in Cushing's syndrome. Biochemical data obtained from routine blood chemistry in 10 patients with Cushing's syndrome were compared with those for 15 patients with histologically verified fatty liver. We found an absence of a decreased GOT/GPT ratio, low normal choline esterase and increased lactic dehydrogenase activities together with lowered serum protein and albumin, and increased blood sugar and total cholesterol in Cushing's syndrome when compared with those of fatty liver cases. These data and additional findings in liver histology obtained from one patient with Cushing's syndrome due to adrenocortical carcinoma indicated that fatty changes in the liver were not frequently encountered in Cushing's syndrome. These abnormal biochemical data might be a way of distinguishing Cushing's syndrome from fatty liver.
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PMID:Abnormal blood chemistry data in Cushing's syndrome: comparison with those for fatty liver. 653 90

The researches of Chiodi, Altland et Al. have shown fatty liver degeneration in hypoxic suckling rats. These alterations produced death within 30 days of life. In order to better understand the relationships between the fatty metabolism and hypoxia, we have studied total plasmatic lipids and cholesterol, glutamic-oxaloacetic and glutamic-pyruvic transaminase in the albino rats raised under normobaric hypoxia to avoid effects linked to barometric modifications. Total plasmatic lipids are reduced in hypoxic animals. In the others parameters we have not shown significant changes.
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PMID:[Initial observations on lipid metabolism in the albino rat raised under normobaric hypoxic hypoxia]. 688 52

We investigated the effect of Probucol in preventing fatty liver in monosodium-L-glutamate (MSG) treated obese mice and control mice fed a high fat diet. MSG mice became significantly obese 9 weeks after birth with higher levels of serum blood glucose, total cholesterol, HDL-cholesterol, GPT, and cholinesterase, and had greater triglyceride contents in their livers relative to control mice. Morphologically, MSG obese mice also had a marked fatty liver. Administration of Probucol mixed with the high fat diet for 2 weeks significantly decreased the serum levels of total cholesterol and HDL-cholesterol, and liver triglyceride contents in both MSG and control mice. Morphologically, the livers were less fatty after Probucol treatment. These results suggest that Probucol prevents the development of fatty liver, and in addition reduces hypercholesterolemia.
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PMID:Probucol prevents the progression of fatty liver in MSG obese mice. 755 75


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