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)

A series of clinical-chemical tests was conducted in 68 schizophrenic out-patients under long-term neuroleptic medication, with particular consideration of the hepatic metabolism, i.e.: Erythrocyte sedimentation rate, alpha 1-glycoprotein, ceruloplasmin, fibrinogen, GPT, GOT, gamma-GT, total protein and serum-protein-electrophoresis. Furthermore, the glucose tolerance tests was carried out. In 44% of the patients an increased erythrocyte sedimentation rate and positive correlations with increased fibrinogen values were found. Increased gamma-GT-values were proven in 33% of the patients; they correlated positively with the increased GPT-and/or GOT-values as well as with pathological glucose tolerance values. Overweight of more than 10 kilos was found in 46% of the patients. A significant correlation between overweight and pathological glucose tolerance values existed. The results were interpreted as consequence of a light fatty liver.
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PMID:[Clinical-chemical studies in schizophrenic out-patients under neuroleptic long-term treatment with particular consideration of the hepatic metabolism (author's transl)]. 88 47

Opsonic glycoprotein, alpha 2-HS-glycoprotein concentration was studied in the serum of 753 patients with various hematological, malignant, immunological, metabolic, endocrine and liver diseases and 68 healthy controls. Decreased serum alpha 2-HS-glycoprotein levels were detected in patients with acute leukemias, chronic granulocyte and myelomonocyte leukemias, lymphomas, myelofibrosis, multiple myeloma, metastatizing solid tumors, systemic lupus erythematosus, rheumatoid arthritis, acute alcoholic hepatitis, fatty liver, chronic active hepatitis, liver cirrhosis, acute and chronic pancreatitis, and Crohn's disease. Elevated levels were measured in patients with B and NANB/C hepatitis. Further decreased levels were observed in some groups with secondary infections. Serum alpha 2-HS-glycoprotein levels are affected by many factors, influencing the synthesis and elimination of the protein. The detection of serum alpha 2-HS-glycoprotein concentration has no specific diagnostic value as a marker for tumors or other diseases, however, its determination can be useful for the assessment of a non-specific regulator of the host defence.
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PMID:[Diagnostic value of the determination of serum alpha2-HS-glycoprotein]. 140 55

Two brothers presented with olivopontocerebellar atrophy of neonatal onset. The clinical features (failure to thrive, hypotonia, liver disease, effusions, and visual inattention) were similar to those of the four cases already reported, as were the necropsy findings of olivopontocerebellar atrophy, hepatic steatosis and fibrosis, and microcystic renal changes. The clinical similarities between this and the disialotransferrin developmental deficiency syndrome were noted. The characteristic abnormality of serum transferrin found in the latter syndrome was also found in the two cases reported here. We suggest that both syndromes are caused by the same, or related, defects in glycoprotein metabolism.
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PMID:Olivopontocerebellar atrophy of neonatal onset and disialotransferrin developmental deficiency syndrome. 192 7

The article reviews the effect of diabetes on the pharmacokinetics and pharmacodynamics of drugs in humans. For most drugs which cross the gastrointestinal wall by passive diffusion, oral absorption is unlikely to be affected by diabetes, although a delay in the absorption of tolazamide and a decrease in the extent of absorption of ampicillin have been reported. Subcutaneous absorption of insulin is more rapid in diabetic patients, whereas the intramuscular absorption of several drugs is slower. The binding of a number of drugs in the blood is reduced in diabetes, which may be due to glycosylation of plasma proteins or displacement by plasma free fatty acids, the level of which is increased in diabetic patients. Plasma concentrations of albumin and alpha 1-acid glycoprotein do not appear to be changed by the disease. The distribution of drugs with little or no binding in the blood is generally not altered, although the volume of distribution of phenazone (antipyrine) is reduced by 20% in insulin-dependent diabetes mellitus (IDDM). In contrast to animal studies, the metabolic clearance of most drugs in humans appears to be unaffected or slightly reduced by the disease. The presence of fatty liver in non-insulin-dependent diabetes mellitus (NIDDM) may contribute to a reduced hepatic clearance, whereas decreased binding in the blood may cause an increase in clearance. The effect of diabetes on hepatic blood flow in humans appears to be unknown. Diabetes affects kidney function in a significant number of diabetic patients. During the first 10 years after the onset of the disease, glomerular filtration is elevated in these patients. Thus, the renal clearance of a number of antibiotics has been shown to be increased in diabetic children. As the disease progresses, renal function is impaired and glomerular function declines from the initial elevated state. In diabetic adults the renal clearance of drugs either is comparable with that found in nondiabetic individuals or is reduced. A limited number of studies have been conducted comparing the dose-response of cardiovascular drugs in diabetic patients with that in nondiabetic controls. Decreased, increased and unchanged responses have been reported. It is apparent that in some cases an altered response may be observed for a drug when administered to a diabetic patient compared with a similar nondiabetic individual. At the present time, it is not possible to ascertain whether these studies reflect true pharmacodynamic changes or merely alterations in pharmacokinetics.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effects of diabetes mellitus on pharmacokinetics and pharmacodynamics in humans. 204 31

C4b-binding protein (C4bp), a glycoprotein involved in regulating the classical pathway of the complement system, binds the activated form of C4b and accelerates the decay rate of the C4b, C2a complex. Recently, sequence analysis of the cDNA for proline-rich protein (PRP) demonstrated that PRP is identical with C4bp. We measured the concentration of C4bp in serum by single radial immunodiffusion in patients with various liver diseases. Concentration of C4bp was significantly lower in hepatic cirrhosis (P = 0.001) and higher in fatty liver (P = 0.0002) than the control values, after adjusting for age, sex, and concentration of total cholesterol, triglyceride, and C-reactive protein. Significant positive correlations were observed between the concentration of C4bp in serum and total protein, albumin, cholinesterase level, and lecithin-cholesterol acyltransferase activity. Immunohistochemical analysis of human liver with specific antiserum to human C4bp demonstrated reaction endproducts in the hepatocytes around the central veins. These observations provide evidence that C4bp is synthesized by hepatocytes.
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PMID:Evidence that C4b-binding protein (proline-rich protein) is synthesized by hepatocytes. 204 87

Serum concentration of the aminoterminal peptide of procollagen type III (P III P) and that of the high-molecular-weight glycoprotein laminin P1 (LP1) were determined by a specific radioimmunoassay (RIA) in patients with different chronic liver diseases. Besides the routine laboratory tests, histological verification of the liver samples obtained by needle biopsy and a complex hepatitis B virus marker analysis by RIA (Biomedica-Sorin), or ELISA (Behringwerke, Marburg, FRG) kits were carried out in order to set up the correct clinical diagnosis. In normal controls, the P III P and LP1 concentrations were 7.8 +/- 1.1 ng/ml (n = 10) and 0.08 +/- 0.1 units/ml (n = 7), respectively. Patients with fatty liver (n = 25) showed a significant elevation in P III P concentration (18.6 +/- 2.7 ng/ml). Such an elevation was not unequivocally demonstrated before. In this group of patients LP1 level was also increased (1.4 +/- 0.2 units/ml, n = 10). In liver cirrhosis (n = 51) both P III P and LP1 concentrations were found to be consistently elevated.
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PMID:Determination of the aminoterminal peptide of procollagen type III and laminin P1 in serum of patients with chronic liver disease. 324 55

We measured the concentration in plasma of fibronectin, a recently characterized high molecular weight glycoprotein, in patients with various liver diseases. We found that it was significantly increased in acute hepatitis, fatty liver, all types of chronic hepatitis and liver cirrhosis without clinical evidence of ascites. Only in patients at the decompensated stage of liver cirrhosis, i.e. patients with clinical evidence of the presence of ascites, was it significantly reduced. Based on the immunohistochemical study on biopsy specimens of the liver using anti-human fibronectin antiserum, we suggest a possible correlation of the elevated plasma fibronectin to the wide distribution of specific fluorescence associated with the fibrillar structures in necrotic areas, expanded portal areas or thick fibrous septa in the liver diseases. Accelerated catabolism of plasma fibronectin mediated by increased fibrinolytic activity may contribute to the decrease in the level of plasma fibronectin in severe liver cirrhosis.
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PMID:Distribution of fibronectin in plasma and liver in liver diseases. 703 11

Haptoglobin (Hp), an acute-phase protein, is detected in serum of cows with hepatic lipidosis (fatty liver). To assess the relevance of Hp in fatty liver, induction of Hp was examined, using conditions similar to those involving development of fatty liver in cows. Induction of Hp was achieved by a combination of dexamethasone administration (0.1 mg/kg of body weight) and 2 days' starvation. Haptoglobin appearance in serum was not associated with the increase of alpha 1-acid glycoprotein (a marker for inflammation). This treatment increased serum nonesterified fatty acids concentration and decreased serum triglycerides concentration. Protein kinase C activity was decreased in the cytosolic fractions of liver and mononuclear cells. Reduction of protein kinase C-catalyzed endogenous protein phosphorylation also was observed, particularly in the cytosolic fractions of the tissue and cells. Detection of Hp in serum of cows with fatty liver appears to be explained by the fact that Hp is induced by dexamethasone administration and starvation, which are similar to the condition responsible for fatty liver development. The change of protein kinase C-catalyzed phosphorylation was suggested to be involved in the induction of Hp in cows.
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PMID:Possible involvement of protein kinase C with induction of haptoglobin in cows by treatment with dexamethasone and by starvation. 831 60

Adult male Sprague-Dawley rats were treated with USP-grade L-tryptophan at a level of 250 mg/kg seven times over 14 d or three times over 3 d by gastric gavage. At autopsy liver specimens were prepared for histological study by stains specific for lipids, for glycoprotein and glycogen, and for fine structure by electron microscopy. Liver lipid did not accumulate as a result of tryptophan treatment. In a series of unfed animals, however, liver lipid had accumulated within 24 h of food withdrawal. Tryptophan has been implicated in fatty liver development by several reports that cite each other, but, in all cases but one, unfed animals were used, and the data show that liver lipid was already present in the unfed animals at the beginning of the experiment. Tryptophan has also been cited as causing abnormal liver morphology, but our evidence suggests that such observations are the result of artifact induced by frozen section preparation and not the result of tryptophan treatment. Our experiments indicate that tryptophan administered to rats at dosages in excess of those recommended for humans does not induce fatty liver or other morphological changes detectable by the methods described.
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PMID:Rat liver is not damaged by high dose tryptophan treatment. 848 97

Sera from 14 normal control subjects, 30 patients with alcoholic liver diseases (fatty liver, n = 8; hepatitis, n = 13; liver cirrhosis, n = 9), 7 controls with chronic hepatitis B, and 8 controls with chronic hepatitis C were masured for their concentrations of antibodies against HepG2 membrane protein by a binding assay utilizing 125I-labeled protein A. When the cut-off level was set as the mean value plus 2 SD of normal control subjects, the incidence of positivity was 75%, 69.2%, and 77.8% in patients with alcoholic fatty liver, alcoholic hepatitis, and alcoholic cirrhosis, respectively. Both the mean serum antibody values and the positive incidence were significantly higher in patients with alcoholic liver diseases than in either the normal controls or in the control patients with chronic hepatitis. Sodium dodecylsulfate polyacrylamide gel electrophoresis of 125I-labeled HepG2 membrane protein precipitated with IgG from patients with alcoholic liver diseases revealed an immunoreactive band at a molecular weight of 78,000 daltons (gp78). The antibody activity remained after immunoabsorption by human liver-specific lipoprotein (LSP) but decreased when HepG2 cells were pre-treated with trypsin or neuraminidase. Consequently, gp78 appears to be a glycoprotein distinct from LSP, and is specifically recognized by IgG from patients with alcoholic liver diseases. This assay may provide a new system to measure autoantibody to hepatocytes in alcoholic liver diseases.
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PMID:Autoantibody against a 78 kDa membrane protein of HepG2 cell in the sera of patients with alcoholic liver diseases. 896 93


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