Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum gamma-glutamyl transpeptidase (gamma-GT) level was estimated in 132 patients with different liver diseases (chronic persistent and chronic active hepatitis, postnecrotic cirrhosis, chronic alcholic hepatitis and alcoholic cirrhosis, cholestasis syndrome, fatty liver, Gilbert disease) and malignancies with and without liver involvement. The gamma-GT levels were compared with the values for serum bilirubin, transaminases (GOT, GPT) and alkaline phosphatase in the same patients. gamma-GT values were normal in chronic persistent hepatitis and increased in chronic active hepatitis. Very high activities were measured in chronic alcoholic cirrhosis in contrast to postnecrotic cirrhosis. gamma-GT proved to be more sensitive than alkaline phosphate as an index of cholestasis and liver involvement in malignancies. It is suggested that gamma-GT activity offers valuable aid in differential diagnostics of liver-diseases. gamma-GT being an inducible enzyme, its activity may be raised by enzyme inducing drugs also in subjects without liver disease.
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PMID:Serum gamma-glutamyl transpeptidase: its clinical significance. 2 44

Acute hydrazine exposure elevated rat liver triacylglycerol content and produced a rapid rise in triacylglycerol production from sn-[1,3-14C]glycerol 3-phosphate by liver homogenate and microsomal fractions. Hydrazine treatment also increased the incorporation of [1,3-14C]glycerol into hepatic triacylglycerol by the intact animal. Homogenates of hepatocyte monolayers exposed to hydrazine in vitro also exhibited an increased capacity to form triacylglycerol from sn-[1,3-14C]glycerol 3-phosphate. Hydrazine-dependent increases in hepatic triacylglycerol production measured in vitro correlated well with an increase in microsomal phosphatidate phosphohydrolase (EC 3.1.3.4) activity. Therefore, the fatty liver associated with hydrazine exposure may be explained in part by a rise in the enzymatic capacity of hepatic triacylglycerol biosynthesis.
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PMID:Effect of hydrazine exposure on hepatic triacylglycerol biosynthesis. 48 20

Influence of the infusion of amino acid solutions on metabolic changes caused by parenteral nutrition with fructose. In eleven unconscious polytraumatized patients of the intensive care station, intravenous infusions with fructose (0.5 g/kg bodyweight and hour) were performed. During the last 24 hours of the 72 hours infusion period, amino acid solutions (1.0 g/kg bodyweight and 24 hours) were given in addition to fructose. The investigations were initiated after an eight hour "starvation period" preinfusion. During this time only electrolytes were given. For comparison 48 hours intravenous infusions with fructose (0.5 g/kg B.W. and hour) were performed with six healthy volunteers. In both groups of subjects the intravenous fructose was metabolized very well, renal losses were less than 2% of the whole amount given. Considering the metabolic healthy volunteers, the blood glucose concentration remained unaltered despite the high dosage carbohydrate infusion. The patients of the intensive care station showed a slight increase of blood glucose values which were elevated already before infusion. Additionally, during fructose infusions, the increase in blood lactate concentration was more pronounced in the intensive care patients than in healthy volunteers. However, in contrast to the healthy volunteers, no increase in serum bilirubin concentration and only a slight increase in serum uric acid concentration was observed in the intensive care patients, despite the high-dose fructose infusion for 72 hours. Additionally, the fructose-induced hypertriglyceridemia was of a minor degree in the intensive care patients. In volunteers the increase in triglyceride concentration was 200% in 48 hours, whereas only a 50% increase was observed in intensive care patients during 72 hours. The pronounced nitrogen sparing effect of fructose in healthy volunteers was not seen in the intensive care patients to the same degree. The most prominent side effect of the fructose infusions in intensive care patients was the strong decrease in serum phosphate concentration seen in some patients. The additional infusion of amino acid solutions lead to a further diminution of the slight alterations caused by fructose infusions. In conclusion, it can be stated that total parenteral nutrition with fructose and amino acid solutions is possible in intensive care patients without danger of side effects. However, it should be mnetioned that hyperalimentation can cause fatty liver.
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PMID:[Effect of amino acid infusions on fructose-induced chemical blood changes in intensive care patients]. 82 61

Double-labelled phosphorylethanolamine with a [32P]//[14IA1 ratio of 1 was incubated in vitro with rat liver slices prepared from control and ethanol-intoxicated rats, and the radioactivity measured at given time intervals in liver ethanolamine, phosphorylethanolamine, phosphatidylethanolamine and phosphatidylcholine. Evidence is presented that after 10 and 15 minutes phosphorylethanolamine enters the slices as an intact molecule, which is directly converted into lipid forms by the Kennedy's pathways. At longer times a hydrolysis of the ester occurs which lowers considerably the theoretical [32P]/[14C]ratio. Fatty liver slices produced by acute ethanol intoxication uptake from the medium more phosphorylethanolamine than controls, and hydrolyze less efficiently than controls the phosphoric ester to ethanolamine and inorganic phosphate.
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PMID:The effect of acute ethanol administration on phosphorylethanolamine uptake and metabolism in rat liver slices. 89 14

Serum 25-hydroxyvitamin D3 levels were determined in chronic hepatic diseases by a radioreceptor assay and correlated with serum albumin, calcium and anorganic phosphate, 25-hydroxyvitamin D3 serum levels were significantly lower inall chronic hepatic diseses compared to normals. The low levels are correlated with the degree of parenchymal damage, not with the etiology of hepatic disease. In alcoholic liver disease thus 25=hydroxyvitamin D3 levels are significantly lower when cirrhosis is present than in mere fatty liver. Anorganic phosphate and calcium were close to the lower range of normal and significantly lower than in the control group studied.
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PMID:Serum 25 -- hydroxyvitamin D3 levels in patients with liver disease. 90 74

Hypertriglyceridemia and fatty liver are common lipid abnormalities associated with Gram-negative sepsis. Fish oils have been shown to have beneficial effects in reducing plasma triglycerides (TG). This study was designed to investigate whether fish oils would prevent the elevation of plasma TG and the accumulation of liver lipids during sepsis. One group of rats was fed a 10% menhaden oil diet and the other group was fed a 10% corn oil diet for 14 days. On the 14th day, sepsis was induced by injecting the rats with 8 x 10(7) live Escherichia coli colonies/100 g of body weight and the rats were fasted for 22 hours. The liver composition of total lipids and TG in the septic rats prefed the fish oil was lower than in the septic rats prefed the corn oil. In the rats adapted to the corn oil diet, lipids accumulated in the livers of the septic rats in comparison with the control rats. Hepatocytes isolated from the septic rats adapted to the corn oil diet showed an increased esterification of [1-14C]palmitate into TG and phospholipids than hepatocytes from the control rats. Feeding the fish oil diet instead of the corn oil diet before inducing sepsis reduced TG, cholesterol, and phospholipid synthesis by 58%, 79%, and 71%, respectively. The rise in TG synthesis in the septic rats prefed the corn oil diet was associated with an 89% increase in the activity of phosphatidate phosphohydrolase. There was no significant difference in the activities of glycerol-3-phosphate acyltransferase and phosphatidate phosphohydrolase between control and septic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adaptation to a fish oil diet before inducing sepsis in rats prevents fatty infiltration of the liver. 164 Jun 34

The hepatic steatosis observed in the influenza B virus mouse model of Reye syndrome has been attributed to infectious virus or, alternately, to decreased food intake in the virus-treated mice or impurities in the virus preparation. To resolve this issue, 4- to 6-wk-old male Balb C mice were given, by intravenous injection, 12,800 hemagglutination units of influenza B Lee/40 virus in phosphate buffered saline/1% bovine serum albumin using virus prepared by ultra-centrifugation from infected allantoic fluid, by sucrose density-gradient purification of virus prepared by ultracentrifugation from infected allantoic fluid or by irradiation of virus prepared by ultracentrifugation from infected allantoic fluid to inactivate virus. The infectivity titer of virus prepared by ultracentrifugation from infected allantoic fluid was much higher than that of sucrose density-gradient purified virus prepared from infected allantoic fluid: 50% egg infectious dose for virus prepared by ultracentrifugation from infected allantoic fluid was 3.9 x 10(4)/hemagglutination unit vs. 8.7 50% egg infectious dose/hemagglutination unit for sucrose density-gradient purified virus prepared from infected allantoic fluid. Control mice received phosphate-buffered saline/1% bovine serum albumin or uninfected allantoic fluid diluted in phosphate-buffered saline/1% bovine serum albumin. Mice were fasted to eliminate dietary variation, and livers were obtained 36 hr after virus administration. Of the above treatments, only virus prepared by ultracentrifugation from infected allantoic fluid caused clinical illness and increased hepatic triglycerides (p less than 0.02) compared with controls. Hepatic triglycerides in virus prepared by ultracentrifugation from infected allantoic fluid correlated with histopathological vacuolization scores (r = 0.5773; p less than 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of influenza B virus in hepatic steatosis and mitochondrial abnormalities in a mouse model of Reye syndrome. 184 48

We evaluated the effects of phenobarbital, an inducer, on plasma glucose and serum immunoreactive insulin levels and on hepatic glucose and drug metabolism using an animal model of non-insulin dependent diabetes mellitus. Genetically obese (ob/ob) mice, characterized by hyperglycaemia, hyperinsulinaemia, fatty liver and obesity were selected. The impairment of diabetic state with age was associated with increased activities of NADPH producing enzymes, whereas mixed function oxidase system remained unaltered. Phenobarbital reduced serum immunoreactive insulin and plasma glucose levels and decreased gluconeogenesis. Hepatic glucose phosphorylating enzyme activity increased and glucose releasing enzyme activity decreased. The demand for NADPH in drug oxidation reactions, caused by the induction phenomenon, was reflected in the elevated activities of the NADPH producing enzymes in pentose phosphate pathway and in the activities of isocitrate dehydrogenase and malic enzyme from mitochondrial oxidation reactions. Glucose metabolism of lean littermates indicated that phenobarbital induction normalizes impaired intracellular glucose handling but leaves normal glucose metabolism unaltered. Hepatic glucose production rate was related to plasma glucose, NADPH producing enzyme activities and cytochrome P450 content in the obese and lean mice.
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PMID:Effects of enzyme induction therapy on glucose and drug metabolism in obese mice model of non-insulin dependent diabetes mellitus. 250 Oct 61

31P NMR was used to study the erythrocytes of three patients who exhibited a familial multisystem disease characterized by fatty liver, diabetes and nonspherocytic hemolytic anemia of unknown etiology. 31P NMR measurements disclosed an abnormally high level of intracellular inorganic phosphate (Pi) and an abnormally low level of ATP in the erythrocytes 6 h after blood withdrawal from proband (I-1). This finding suggested that ATP was markedly decreased in the red cells of this proband, as compared with those of normal subjects. Time-dependent changes of 31P NMR spectra of the erythrocytes from the two daughters (II-1, II-2) of the proband demonstrated clearly an enhanced decomposition of ATP with a concomitant increment of Pi. Several ATP-consuming enzymes in erythrocytes, such as those in the Embden-Meyerhof system, pentose phosphate pathway enzymes, Na+, K(+)-ATPase and Ca2+, Mg2(+)-ATPase, were within normal limits of activity, but Mg2(+)-ATPase was drastically above the normal limit. The Mg2(+)-ATPase activity was 3 times higher in the red cell membranes of these patients than in those from normal subjects.
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PMID:An interesting syndrome of hemolytic anemia, degeneration of the liver and diabetes associated with a high red cell Mg-ATPase, detected by 31P NMR spectroscopy. 253 4

The metabolic effects of ethanol are due to a direct action of ethanol or its metabolites, changes in the redox state occurring during its metabolism, and modifications of the effects of ethanol by several nutritional factors. Ethanol causes hyperglycemia or hypoglycemia depending whether or not glycogen stores are adequate, inhibits protein synthesis, and results in a fatty liver and elevations in serum triglyceride levels. Increases in serum lactate, results from the increased reduced nicotinamide-adenine dinucleotide/nicotinamide-adenine dinucleotide + (NADH/NAD+) ratio, and hyperuricemia probably occurs owing to the increased turnover of adenine nucleotides after ethanol ingestion. Ethanol decreases thiamine absorption and decreases the enterohepatic circulation of folate. Acetaldehyde, the major metabolite of ethanol, increases the degradation of pyridoxal 5'-phosphate by displacing it from its binding protein and making it susceptible to hydrolysis by membrane-bound alkaline phosphatase. Chronic ethanol administration also results in decreased vitamin A stores and reduced bone mass and blood levels of 25-hydroxyvitamin D. The mechanism whereby ethanol affects these vitamins and their associated enzymes is unknown.
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PMID:The effect of ethanol and its metabolites on carbohydrate, protein, and lipid metabolism. 329 39


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