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 high incidence of subclinical fatty liver-haemorrhagic syndrome (FLHS) was found in three flocks of laying hens in which deaths from FLHS had occurred. There was so significant difference between the affected hens and the remainder of the block in egg production or quality, but the former were more obese and had higher concentrations of lipids in their livers, suggesting a pathogenic relationship between hepatic steatosis and haemorrhage. Soluble protein tended to accumulate with the fat in the livers. Reticulolysis had occurred in over half the haemorrhagic livers examined. Histological examination and DNA estimations provided no evidence of generalised hyperplasia. From the composition of the liver lipids it was concluded that the steatosis resulted mainly from an increase in lipogenesis from dietary carbohydrate. Lipid levels in the plasma were weakly correlated with those in the liver. No change was detected in the plasma protein pattern.
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PMID:Pathological and biochemical observations on subclinical cases of fatty liver-haemorrhagic syndrome in the fowl. 62 3

Because of the frequent reports of hepatic toxicity associated with long-term administration of methotrexate, a rat model was developed utilizing daily methotrexate administration. This model revealed an incidence of fatty metamorphosis of over 80 percent, atrophy and necrosis of 30 percent, and fibrosis of 10 percent. Fatty liver changes did not differ substantially from control animals in those animals receiving long-term thydroxyurea, an agent which, like methotrexate, inhibits DNA synthesis but unlike methotrexate, does not impair methylation reactions. Because choline has a lipotropic effect and because its synthesis requires methylation, an attempt was made to block the liver toxicity of methotrexate by simultaneous administration of choline. Animals so treated did not show the pathologic changes in the liver characteristic of methotrexate treatment alone. Furthermore, the accumulation of triglycerides in the liver which was characteristic of methotrexate administration was markedly reduced in those animals receiving choline. These data strongly suggest that, in the rat model, methotrexate produced liver toxicity by virtue of an effect other than inhibition of DNA synthesis; and that this toxicity can be blocked without impairing methotrexate effect on bone marrow by the administration of choline, a lipotropic agent requiring methylation for its synthesis. It is suggested that these results may have implications for human therapeutic situations involving long-term administration of methotrexate.
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PMID:Choline antagonism of methotrexate liver toxicity in the rat. 84 Jan 63

Lymphocyte proliferation inhibitory factor (PIF) was determined in the supernatants of PHA-stimulated lymphocytes from patients with alcoholic liver disease. PIF was assayed by determining inhibition of DNA synthesis in WI-38 human lung fibroblasts. A two-fold greater inhibition in thymidine incorporation into DNA by lung fibroblasts was observed in supernatants of PHA stimulated lymphocytes from patients with alcoholic hepatitis or active Laennec's cirrhosis as compared with that found in control subjects or patients with fatty liver. It is suggested that decreased liver cell regeneration seen in some patients with alcoholic hepatitis may be due to increased elaboration of PIF.
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PMID:Lymphocyte proliferation inhibitory factor (PIF) in alcoholic liver disease. 100 Aug 81

Rats were fed a high cholesterol, olive oil diet for one or seven weeks. The resulting hypertrophic fatty livers were analyzed for lipids, nucleic acids, and connective tissue components. The cholesterol and neutral glyceride contents of liver increased approximately 30-fold during the first week while phospholipids remained almost unchanged. After seven weeks the accumulation of cholesterol was further increased and the content of phospholipids enhanced. The total amounts of DNA and RNA rose with increasing weight of fatty liver. In seven weeks the diet caused a marked increase in hepatic collagen and glycosaminoglycans. The synthesis of collagen was increased in fatty liver slices after both one and seven weeks of the experiment. Fatty liver produced by this lipid diet is suggested as a suitable model for studying the mechanism by which lipids stimulate hepatic fibroblasts.
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PMID:Effect of high cholesterol, olive oil diet on the lipids and connective tissue in rat liver. A biochemical study. 100 61

The fatty liver and hypolipidemia caused by aflatoxin B1 (AFB1) were studied in male Sprague-Dawley rats fed Purina Rat Chow with or without L-carnitine supplement for 6 weeks. In Experiment 1, the rats (n = 20) were divided into four groups, i.e., nonsupplemented control (NSC), nonsupplemented AFB1 (NSA), carnitine supplemented control (CSC), and carnitine supplemented AFB1 (CSA). The NSA and CSA groups were given an oral dose of [3H]AFB1 (1 mg/kg) 6 hr before kill. In Experiment 2 (n = 10) there were only NSA and CSA groups and they were killed 24 hr post-AFB1 administration. Hepatic and plasma concentrations of total lipid, triglycerides, AFB1-macromolecules adducts and urinary excretion of AFB1 were determined. Carnitine supplementation ameliorated AFB1-induced hepatic steatosis and hypolipidemia. Supplementary carnitine reduced covalent binding of AFB1 to hepatic DNA, RNA, and protein. The carnitine effect was more pronounced after 24 hr than after 6 hr of AFB1 treatment. We conclude that supplementary carnitine suppressed AFB1-induced fatty liver and AFB1-macromolecule adduct formation in the rat.
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PMID:Suppression of aflatoxin B1-induced lipid abnormalities and macromolecule-adduct formation by L-carnitine. 138 May 53

The clinical specifity of an intraparticular virus-DNA of 5001 Bp associated with non-A, non-B hepatitis (HNANB) was evaluated. Investigations were done in liver biopsies and lymphocytes in 173 patients having acute or chronic HNANB (n = 107) or liver diseases of other etiology (n = 66). The sensitivity of the test system (polymerase chain reaction, southern-transfer, DNA-hybridisation with synthetic oligonucleotides) was less than 100 virus particles per probe. In all patients with acute HNANB (n = 5) (parenteral mode of infection) the DNA was found in 100% in liver and lymphocytes, and in 22 of 27 patients with acute sporadic HNANB. HNANB associated substance (HNANB-AS) (1.3 g/ml CsCl) excreted with feces was found in 50%, and 29.6%, respectively. In chronic HNANB the DNA was found in 83.3% in the liver (n = 42) and in 56.7% in lymphocytes (n = 30). The HNANB-AS was found in 45.6% (n = 68). In liver diseases with other etiologies as HNANB-infection (e.g. HBV, HAV, cholestasis, HBsAg pos.-liver cirrhosis) (n = 33) the DNA was found neither in liver biopsies nor in lymphocytes. In liver diseases of uncertain etiology, but with NANB-infection under discussion (e.g. nonspecific reactive hepatitis, fatty liver, HBV neg liver cirrhosis) the DNA was found in the liver in 24% (n = 25) and in lymphocytes in 40% (n = 5). In patients with clinically resolved HNANB no DNA was found in liver and lymphocytes (n = 5). All stools were negative for HNANB-AS in the latter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical studies of the specificity of detecting viral DNA in non-A, non-B hepatitis in liver tissue and lymphocytes]. 170 May 57

Rats fed an elemental, enteral diet (STD) developed pancreatic atrophy and hepatic steatosis following 60% jejunoileal intestinal resection. An isonitrogenous, isocaloric 2 g/100 ml glutamine-supplemented diet (GLN) significantly attenuated the development of pancreatic atrophy and hepatic steatosis associated with elemental feeding. Pancreatic weight, DNA, and protein were 27, 22, and 40% increased, respectively, in GLN animals. The pancreata of all animals appeared normal by light and electron microscopic examination. GLN animals had 12% less total liver wet weight, 3% less hepatic water content, and 47% less hepatic fat relative to STD rats. Histologic examination of the liver revealed extensive centrilobular fatty vacuolization in STD animals whereas GLN rats had normal looking hepatic parenchyma. Glutamine should be viewed as an important nutrient in elemental diets with trophic effects on the pancreas and protective effects against the development of hepatic steatosis.
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PMID:Glutamine prevents pancreatic atrophy and fatty liver during elemental feeding. 197 Oct 31

Infusion of total parenteral nutrition (TPN) with excess carbohydrate calories leads to hepatic steatosis in rats and is associated with an elevated portal insulin/glucagon molar ratio. Previously we have shown that adding glucagon to TPN prevents and reverses hepatic steatosis in rats, possibly by increasing hepatic lipid export. It has been reported that steatosis is eliminated in rats by the addition of L-glutamine to TPN. In this study, we examined the effect of glutamine on portal insulin and glucagon levels and the development of hepatic steatosis. Adult rats (n = 19) received internal jugular catheters: Group 1 (n = 6), saline (3 cc/hr) and chow ad libitum; Group 2 (n = 7), 25% dextrose base TPN; Group 3 (n = 6), 25% dextrose base TPN with 2% glutamine. The infusion rate of TPN was 1.2 cc/100 g body wt/hr. Daily nitrogen balance was determined and at 7 days, portal venous blood was drawn for insulin and glucagon radioimmunoassay, livers were removed for histology and lipid content determination, and the small intestines were removed for mucosal protein and DNA content determination. Panlobular vacuolization of the hepatocytes was noted on histology in Group 2 (TPN) while Group 1 (chow) and Group 3 (TPN + glutamine) showed normal liver morphology. Hepatic lipid content was significantly elevated in Group 2 (P less than 0.05). The portal insulin/glucagon molar ratio was increased because of excessive portal venous insulin in Group 2 (TPN). In contrast, portal glucagon was significantly elevated while the insulin/glucagon ratio and hepatic lipid content did not increase above control levels in the glutamine-supplemented Group 3 rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Addition of L-glutamine to total parenteral nutrition and its effects on portal insulin and glucagon and the development of hepatic steatosis in rats. 211 67

Liver fatty acid binding protein (L-FABP) is the principal target protein of the hepatic carcinogen N-(2-fluorenyl)acetamide (2-acetylaminofluorene) in rat liver. In addition, the cyclopentenone prostaglandins (PG), PGA, PGJ2, and delta 12-PGJ2, inhibit the growth of many cell types in vitro. This report describes the preferential binding of the growth inhibitory prostaglandins by L-FABP and the reversible inhibition of thymidine incorporation into DNA by PGA2 and delta 12-PGJ2 in primary cultures of purified rat hepatocytes. As a model ligand, [3H]PGA1 bound to L-FABP specifically, reversibly, rapidly, and with high affinity. Its dissociation constants were 134 nM (high affinity) and 3.6 microM (low affinity). The high-affinity binding of [3H]PGA1 was 9- and approximately 13-fold more avid than the binding of the conventional fatty acid ligands, oleic acid and arachidonic acid, respectively. The abilities of different prostaglandins to compete with the high-affinity binding of [3H]PGA1 correlated with their growth inhibitory activities reported previously and here. The growth inhibitory cyclopentenone prostaglandins (PGA1, PGA2, delta 12-PGJ2, and PGJ2) were the best competitive ligands, intermediate competitors were the weak growth inhibitors PGE1 and PGD2, and the poorest competitors were PGE2 and PGF2 alpha, which stimulate rather than inhibit DNA synthesis in rat hepatocytes in primary culture. The in vitro actions of L-FABP are compatible with those of a specific and dissociable carrier of growth inhibitory prostaglandins in rat hepatocytes and suggest that the carcinogen may usurp the cellular machinery of the growth inhibitory prostaglandins.
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PMID:Preferential binding of growth inhibitory prostaglandins by the target protein of a carcinogen. 225 Dec 82

A previously healthy 35-year-old woman was seen at 37 weeks' gestation with a 10-day history of fever, vomiting, diarrhea and malaise. Serum laboratory findings included elevation of serum bilirubin and AST, prolongation of serum prothrombin time and a positive monospot. A tentative diagnosis of acute fatty liver of pregnancy was made, and a healthy male infant was delivered by emergency cesarean section because of fetal distress. Over the subsequent 3 days, acute progressive oliguric renal failure, disseminated intravascular coagulation, hypoglycemia requiring intravenous dextrose infusion and pancreatitis developed; her mental status progressed to stage III encephalopathy. Quantitative computed tomography estimated the liver volume to be 770 cm3. The decision to proceed with orthotopic liver transplantation was made on the basis of progressive clinical deterioration despite aggressive support and because of her small liver size. After transplant, the patient's multisystem failure rapidly reversed. Histopathological examination of the native liver demonstrated predominantly zone 3 microvesicular steatosis with characteristic ultrastructural changes consistent with acute fatty liver of pregnancy. Southern blot analysis for Epstein-Barr virus DNA was negative. We conclude that orthotopic liver transplantation should be considered for the small group of patients with fulminant hepatic failure associated with acute fatty liver of pregnancy who manifest signs of irreversible liver failure despite delivery of the fetus and aggresive supportive care.
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PMID:Fulminant hepatic failure caused by acute fatty liver of pregnancy treated by orthotopic liver transplantation. 240 63


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