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 plasma concentrations of estrogens as well as their relationship to testosterone are determined in male patients suffering from fatty liver, chronic hepatitis and cirrhosis of the liver. By stimulation and suppresion tests the contribution of the adrenal gland and the testes to the elevated estrogens are investigated, demonstrating that enhanced peripheral conversion of androgens to estrone rather than to estradiol appears to be more effective in sustaining plasma levels in hepatic cirrhosis. Futhermore, the effect of testosterone application was studied in male patients with alcohol-induced cirrhosis of the liver in order to realize possible side-effects of an androgenic substitution therapy. It is concluded that clinical signs of hyper-estrogensim and hypoandrogenism in male patients with hepatic cirrhosis may in part be attributed to the increase of estrogens and the decrease of total and free testosterone, as is best shown by the ration of the heterosexual hormones which are grossly shifted in favour of the estrogens.
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PMID:Plasma-estrogens and liver cirrhosis. 22 6

Triglyceride and cholesterol concentrations in whole serum and in the serum lipoprotein fractions were measured during the course of hospitalization in six patients with Reye syndrome, four of whom survived. Very low density lipoprotein (VLDL) triglycerides were significantly lower on admission than on the last day of hospitalization. However, no VLDL triglyceride value was below the normal range. Triglyceride transport was increased in low density lipoprotein (LDL) and high density lipoprotein (HDL) fractions. LDL and HDL cholesterol concentrations were low on admission and decreased further during hospitalization. The changes in LDL and HDL cholesterol concentrations were more severe among nonsurvivors. No HDL cholesterol was detected in nonsurvivors on the last day of hospitalization. These results suggest that decreased VLDL triglycerides may not play an important role in the development of fatty liver and that decreased LDL and HDL cholesterol concentrations may be of prognostic value in Reye syndrome.
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PMID:Triglyceride and cholesterol concentrations in whole serum and in serum lipoproteins in Reye syndrome. 22 24

The sequential pattern of lipid accumulation and associated biochemical changes were studied in two commonly used experimental models of nutritional fatty liver in rats. Female rats were maintained for 8 weeks on high fat, low protein diets containing adequate methionine and choline, and drinking water ad libitum (Diet 1), or deficient in methionine and choline and containing 20% ethanol as a substitute for drinking water (Diet 2). Histologically, there was a progressive increase in liver lipids, mainly in the periportal areas. Occasional foci of liver cell necrosis with lipogranuloma formation occurred in areas of severe fatty change. These changes appeared earlier and were more marked in rats maintained on Diet 2. Electron micrographs revealed large lipid droplets in the liver cells, which sometimes contained myelin figures. The mitochondria were enlarged, distorted and appeared as amorphous structures with disorientated cristae in rats on Diet 1, whereas they had a condensed conformation in rats maintained on Diet 2. Rough endoplasmic reticulum was fragmented and degranulated particularly in rats on Diet 1, and smooth endoplasmic reticulum showed hyperplasia and vesiculation in rats on Diet 2. There was a progressive increase in the total liver lipids and triglycerides in both the groups of rats. This fatty change was accompanied by a significant increase in hepatic 3-hydroxybutyrate, acetoacetate, malate, 2-oxoglutarate, citrate, lactate, ammonia, glutamate, alanine and aspartate, and a significant decrease in oxaloacetate, urea and glucose concentrations. The mass action ratios for alanine aminotransferase, aspartate amino transferase, and glutamate dehydrogenase, generally moved in a parallel direction. Hepatic ATP content was considerably reduced accompanied by a decrease in [ATP]/[ADP] ratios and a significant increased in [lactate]/[pyruvate] and [3-hydroxybutyrate]/[acetoacetate] ratios. There was a corresponding decrease in the [NAD+]/[NADH] ratios both in the cytoplasmic and mitochondrial compartments. These biochemical changes were particularly severe in rats maintained on Diet 1 and Diet 2 for 8 weeks. There was a very good relationship between impaired mitochondrial and endoplasmic reticulum functions, redox and phosphorylation states, and the relevance of their changes to the fate of fatty liver cells.
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PMID:Lipid accumulation in the rat liver: a histological and biochemical study. 23

An initial description of the alcoholic head trauma triad (fatty liver, acute pneumonia and acute subdural hematoma) is presented. The basic nosological features and pathophysiological interrelationships are discussed and areas for further study delineated.
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PMID:Alcoholic head trauma triad. 23 76

A case of acute fatty liver of pregnancy (obstetric acute yellow atrophy or acute fatty metamorphosis of the liver) is reported in which cesarean section was made and both mother and child survived. The authors suggest that the prognosis was improved by rapid termination of pregnancy. The course of the disease, differential diagnosis, treatment and prognosis are discussed.
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PMID:Acute fatty liver of pregnancy with survival of mother and child: a case report. 26 60

A new fatty liver model is described in which heredity plays a major role. A marked fatty liver develops when the homozygous mutant Zucker rat (ff or "fatty") is fed a semisynthetic diet enriched in sucrose. Lean littermates do not develop fatty liver on this experimental diet. Even old ff rats do not develop fatty livers on chow; the experimental diet is required. The fatty liver is described, including light microscopic and preliminary electron microscopic observations.
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PMID:Fatty liver induced in Zucker "fatty" (ff) rats by a semisynthetic diet rich in sucrose. 26 52

A new fatty liver model is described in which heredity plays a major role. A marked fatty liver develops when the homozygous mutant Zucker rat (ff or "fatty") is fed a semi-synthetic diet enriched in sucrose. Lean littermates do not develop fatty livers on this experimental diet. Even old ff rats do not develop fatty livers on chow; the experimental diet is required. The fatty liver is described, including light microscopic and preliminary electron microscopic observations.
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PMID:Fatty liver induced in Zucker "fatty" (ff) rats by a semisynthetic diet rich in sucrose. 26 13

A case of idiopathic fatty liver of pregnancy with survival of mother and child is reported. The management of this condition is essentially supportive; coagulation disturbances may require special attention. Maternal survival should be the major consideration and is favourably influenced by early delivery. Fetal monitoring aids obstetric management and may indirectly improve fetal survival. Evidence from the literature suggests that the condition does not usually recur in subsequent pregnancies.
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PMID:Idiopathic fatty liver of pregnancy with maternal and fetal survival. 27 97

The possible influence of a potent enzyme inducer, phenobarbitone, on white phosphorus fatty liver, was studied. Pretreatment by phenobarbitone for four days in white phosphorus poisoned rats provoked a decrease in mortality and an increase in hepatic triglycerides (fatty liver) in male rats. The activity of uridine diphosphoglucuronyl transferase (UDPGT), an inducible enzyme, is not modified by this pretreatment in white phosphorus poisoned rats. The accentuation of white phosphorus fatty liver by phenobarbitone in male rats could be explained by an increased hydroxylation of testosterone, thus counteracting the protective effect of this hormone on fatty liver.
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PMID:Accentuation of white phosphorus induced fatty liver by phenobarbitone in male rats compared to female rats. 28 40

The steatogenic effect on the liver of Rifampicin, a potent inhibitor of the DNA-dependent RNA polymerase in bacteria, was investigated in male and female rats which received either 200 mg or 400 mg of Rifampicin/kg/24 h for 8 days. The determination of total lipids (TL), triglycerides (TG), total cholesterol (TC) and phospholipids (PL) showed a significant increase of TL, TG and TC in the liver at a dose of 400 mg. There was better reproducibility in the male whose blood TG and PL were significantly decreased. These results showed that fatty liver can be induced by very high doses of Rifampicin in rats. A blockage of the very low density lipoproteins (VLDL) biosynthesis and/or secretion can be expected. As a potent steatogenic toxin, alpha-amanitin, is a strong inhibitor of RNA polymerase II in eukariotic cells, a relationship between the RNA polymerase inhibition induced by both of substances and a subsequent inhibition of the biosynthesis of the protein moiety of lipoproteins can be considered. Nevertheless Rifampicin is at present not considered as an inhibitor in eukariotic cells and it will be of great interest to test such a possibility with the high doses used in these experiments, in further work.
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PMID:Fatty liver induced by high doses of rifampicin in the rat: possible relation with an inhibition of RNA polymerases in eukariotic cells. 28 41


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