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)

The activities of several glycosidases (beta-galactosidase, beta-glucosidase, N-acetyl-beta-glucosaminidase) were demonstrated in human bile. The enzyme activities are increased about 100 times after exclusion of bile salts and other small molecular compounds by Sephadex G-50 gel filtration. The use of 4-methylumbelliferyl derivatives as substrates was useful as measurement of the bile enzyme activities are not altered in the presence of bile pigments. Enzyme characteristics of bile glycosidases were determined: pH optimum and isoelectric point. The bile glycosidase activities were also measured in various hepatobiliary disorders (cholelithiasis, cancer of gallbladder, acute hepatitis, liver cirrhosis and fatty liver). The glycosidase activities in bile from patients with liver diseases, as well as with cholelithiasis, were generally decreased. Isoelectric focusing patterns of biliary glycosidases were similar for specimens from patients with hepatobiliary disorders as compared to normal.
Clin Chim Acta 1977 Sep 01
PMID:Bile lysosomal enzymes: characteristics and pathological significance for various hepatobiliary disorders. 1 80

The concentration of beta 2-microglobulin in serum was determined in seventy-one patients with various liver disorders. Elevated values were found in most patients with chronic active or chronic persistent hepatitis and in over 80% of patients with alcohol-induced liver cirrhosis. In contrast, patients with alcohol-induced fatty liver, the serum beta 2-microglobulin concentrations were mostly within the normal range. Significant correlation (P less than 0.001) was noted between the elimination rate of galactose from blood and the serum beta 2-microglobulin concentration in patients with alcoholic liver damage but not in patients with chronic hepatitis. The reasons for the increased S-beta 2-microglobulin concentrations in liver diseases are unknown. Several explanations including a release of beta 2-microglobulin from necrotic liver cells or an increased synthesis of beta 2-microglobulin consequent to inflammation in the liver are possible. Alternatively, raised beta 2-microglobulin levels may reflect the hepatic synthesis during reparative growth.
Scand J Clin Lab Invest 1979 Sep
PMID:Serum beta2-microglobulin in liver disease. 9 2

The mechanism of liver enlargement and anti-fatty liver effect of NKK-105 in the rat were investigated by the mesurement of drug-metabolizing enzyme activities and morphological changes in liver tissue detected using electron microscopy. A single administration of NKK-105(250, 500, 1000 mg/kg, p.o.) induced an apparent increase in liver weight. The elevation of aminopyrine demethylase activity and slight increase in microsomal cytochrome b5 and cytochrome P-450 content were seen with the administration of NKK-105. NKK-105 inhibited lipid peroxide formation in mitochondrial and microsomal fractions. Total lipid content of liver decreased at 12 hr after the administration of NKK-105. Lipid peroxide formation in mitochondrial and microsomal fractions was markedly inhibited by the addition of NKK-105 (1 X 10(-3)M), in vitro. Disarrangement of rough endoplasmic reticulum and increase in smooth endoplasmic reticulum were observed by the administration of NKK-105. The decrease in drug-metabolizing enzymes caused by CCl4 or ethionine was protected in the combination with NKK-105. NKK-105 markedly inhibited the elevation of lipid peroxide formation caused by CCl4 or ethionine. Similar effects on lipid peroxide formation were also obtained in vitro. These results suggest that the enlargement induced by NKK-105 indicates a functional not a toxic response. The inhibition of lipid peroxide formation in mitochondrial and microsomal fractions may thus play an important role in the mechanism of anti-fatty liver effect of NKK-105 on the CCl4 or ethionine-induced fatty liver.
Nihon Yakurigaku Zasshi 1979 Sep
PMID:[Effects of diispropyl 1, 3-dithiol-2-ylidene malonate (NKK-105) on the drug-metabolizing enzymes and fine structure of rat liver (author's transl)]. 12 Feb 99

A survey of routine mortality was carried out on six different broiler sites. A total of 535 individual post mortem examinations was carried out. The chief cause of mortality on all six sites was colisepticaemia. Fatty liver and kidney syndrome caused significant loss on three of the six sites and on three of them a low incidence of an oedema syndrome was of interest. Salmonella senftenberg was isolated during the first four weeks from the intestines of chickens from five of the six sites but on none of them was this occurrence associated with any manifestations of disease. The vaccination procedures against Newcastle disease and infectious bronchitis were not producing adequate immunity against a possible challenge by a virulent virus of either although the administration of the vaccines appeared to be causing stress sufficiently severe to be one of the factors predisposing to a high incidence of colisepticaemia.
Vet Rec 1977 Sep 17
PMID:A survey of "normal" broiler mortality in East Anglia. 33 32

Ninety patients with chronic diffuse liver disease were evaluated with free hepatic venography, wedge hepatic venography, hepatic vein pressure measurements, and liver biopsy. Free hepatic venograms were normal and minimally pruned in patients with hepatic sarcoidosis and fatty liver due to alcohol, and their biopsies showed little or no fibrosis. Pruning of hepatic vein branches on free hepatic venography correlated well with the corrected wedged hepatic vein pressure and with the degree of fibrosis in patients with alcoholic hepatitis, alcoholic cirrhosis, and postnecrotic cirrhosis. Free hepatic venography correlated better with hemodynamic measurements and fibrosis than did wedge hepatic venography. Free hepatic venography is a reliable predictor of the presence and degree of hepatic fibrosis and may be a useful alternative to liver biopsy in patients with clotting disorders.
AJR Am J Roentgenol 1977 Sep
PMID:Hepatic venography and wedge hepatic vein pressure measurements in diffuse liver disease. 40 97

Reye's syndrome (encephalopathy and fatty liver) is generally considered a disease of children. Four patients, aged 16, 18, 19, and 23 years, with Reye's syndrome were initially seen by internists. A viral prodrome followed by vomiting and encephalopathy without focal neurological signs or jaundice clinically suggested Reye's syndrome. Normal findings of CSF examination (except for increased opening pressure), abnormal findings of liver function tests, and increased blood ammonia further supported the diagnosis. None was hypoglycemic. Reye's syndrome was related to influenza B virus in three patients and to Varicella in another. Three patients survived. Reye's syndrome may be seen intially by general practitioners, emergency room physicians, internists, or psychiatrists. The importance of considering this syndrome in the differential diagnosis of unexplained encephalopathy in adults is stressed.
JAMA 1979 Sep 28
PMID:Reye's syndrome in nonpediatric age groups. 48 May 58

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.
Biochim Biophys Acta 1979 Sep 28
PMID:Effect of hydrazine exposure on hepatic triacylglycerol biosynthesis. 48 20

A role for bacterial colonization of the intestines in the pathogenesis of hepatic abnormalities after jejunoileal bypass was sought. Dogs were divided into groups according to the disposition of the bypassed segment; resection (group I), exteriorization as an ileal mucous fistula (group II), and drainage via an ileocolonic anastomosis (group III). Weight loss, abnormalities in liver function, and hepatic steatosis were significantly greater in groups II and III than in group I. Concomitantly, there was a significant increase in the total number of bacterial colony-forming units in groups II and III. Moreover, a greater number of specific anaerobic genera was isolated in group III than in group II. It is concluded that: (1) retention of the bypassed intestinal segment is associated with greater changes in liver function and structure than when the segment is resected; (2) the changes in the liver correlated with bacterial proliferation in the bypassed intestinal segment; and (3) despite a greater number of anaerobic genera in the ileocolostomy than in the mucous fistula, both procedures were associated with hepatic abnormalities.
J Infect Dis 1979 Sep
PMID:Microbial colonization and hepatic abnormalities in jejunoileal bypass with resection, ileal mucous fistula, and ileocolostomy. 50 Nov 49

1. The changes in a number of metabolic measurements brought about by low-biotin diets associated with high and low incidences of fatty liver and kidney syndrome (FLKS) were studied in healthy 4-week-old broiler chicks. 2. Liver pyruvate carboxylase (pyruvate: CO2 ligase (ADP); EC 6.4.1.1) activity was low in birds fed on a diet causing a high incidence FLKS but the addition of fat or protein to this diet, to decrease the incidence of FLKS, increased enzyme activity. 3. Liver weights, blood lactate concentrations, plasma lactate dehydrogenase (L-lactate: NAD oxidoreductase; EC 1.1.1.27) activitvities and values for C16:1 : C18:0 fatty acid in liver, adipose tissue and plasma triglyceride were highest in birds fed on the high-FLKS diet and all measurements were negatively correlated with pyruvate carboxylase activity. 4. Birds with high plasma lactate dehydrogenase activity or triglyceride C16:1 : C18:0 values were the most likely to develop FLKS when fasted. 5. There was no evidence that increased liver weight was associated with increase activities of certain other liver enzymes. 6. It is concluded that FLKS occurs in birds with little or no hepatic gluconeogenic capacity via pyruvate carboxylase as a result of a dietary insufficiency of biotin but that the initiation of the syndrome in probably associated with the inhibition of other pathways of gluconeogenesis.
Br J Nutr 1978 Sep
PMID:Metabolic changes associated with the occurrence of fatty liver and kidney syndrome in chicks. 69 61

Hepatic lipid peroxidation in vivo or in vitro as measured by UV absorption spectra of microsomal lipids or by production of TBA-reacting substances by whole liver homogenates, was studied after acute or during prolonged administration of ethanol. No evidence of peroxidative derangement of liver microsomal lipids in vivo was detected in either experimental situation, while the production of TBA-reacting substances by pooled liver homogenates incubated in vitro appeared slightly increased. Treatment with reduced glutathione (GSH and 2-mercaptopropionylglycine (2-MPG) was able to reduce fatty liver in acute and prolonged ethanol dosing, as well as the production of TBA-reacting compounds. Similar effects were obtained with 3-amino-1,2,4-triazole which was assayed only in acute experiments. By contrast, hepatic triglyceride accumulation induced by a single intoxicating dose of ethanol was not affected by preventive treatment with pyrazole which seemed to act as a pro-oxidant agent as far as the production of TBA-reacting substances is concerned. The role of lipid peroxidation as a pathogenic mechanism for acute and chronic ethanol-induced hepatotoxicity is discussed in relation to the action of anti-oxidant compounds which are active in preventing liver injury. It is concluded that lipid peroxidation is unlikely to be an important mechanism in alcohol hepatotoxicity.
J Pathol 1978 Sep
PMID:Ethanol-induced hepatotoxicity; experimental observations on the role of lipid peroxidation. 72 5


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