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)

Arginine deficiency is known to lead to marked alterations in pyrimidine biosynthesis and the excessive loss of urinary orotic acid. Orotic acid feeding is known to lead to hepatic steatosis. These studies show that arginine deficiency also results in a marked increase in liver lipids in the rat. The majority of the increased liver lipid can be accounted for by triglyceride accumulation. Increased liver lipid infiltration was found to be independent of the sex of the rat. Accompanying this increase was a decrease in serum triglycerides and cholesterol concentrations. Fatty infiltrations induced by arginine deficiency could be reversed by refeeding an arginine enriched diet. Adenine supplementation (0.30%) to the arginine deficient diet also completely prevented the induction of fatty livers. Adenine supplementation resulted in a dramatic increase in urinary orotic acid excretion in the arginine deficient rat. Guanine supplementation (0.5%) to an arginine deficient diet reduced but did not prevent the induction of fatty livers. The similarities of fatty livers induced by arginine deficiency and orotic acid feeding are discussed.
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PMID:Mechanism for fatty liver induction in rats fed arginine deficient diets. 43 Feb 66

Intravenous administration of [1-14C]palmitate to 8-day lactating rats fed a myo-inositol supplemented or deficient diet resulted in rapid labeling of liver triglycerides and phospholipids. Compared with myo-inositol deficient rats, those supplemented with myo-inositol showed a greater loss of isotope from liver triglycerides with a more rapid appearance of isotope in serum triglyceride. Loss of 14C from liver phospholipids was similar for both groups, whereas the appearance of labeled phospholipids in serum was slightly greater for myo-inositol supplemented controls compared with myo-inositol deficient rats. The labeling pattern of liver microsomal triglycerides and phospholipids of the two dietary groups was similar; however, liver microsomal protein was significantly reduced in myo-inositol deficient rats relative to the control group. Concurrent administration of Triton WR-1339 with [1-14C]palmitate resulted in significantly less label accumulation in serum triglycerides of myo-inositol deficient rats compared with myo-inositol supplemented rats. Labeled triglycerides in whole liver and in liver microsomes of myo-inositol supplemented rats turned over more rapidly than those of myo-inositol deficient rats while no significant difference was noted for the [14C]palmitate labeled phospholipid of either source. The incorporation of [guanido-14C]arginine into total liver and serum protein 1 hour after injection of the precursor was similar whether the 14-day lactating dams were myo-inositol supplemented or deficient, but total serum protein specific radioactivity of myo-inositol deficient rats was 66% that of myo-inositol supplemented rats. Thus, the significantly reduced release of hepatic triglycerides appears to be the cause of the fatty liver observed during lactation-dependent myo-inositol deficiency.
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PMID:myo-Inositol deficiency: studies on the mechanism of lactation-dependent fatty liver formation in the rat. 45 2

Extracts of snake venom have been widely used for the treatment of vascular thrombotic diseases, yet the therapeutic mechanism is not clear. The effect of snake venom fractions on atherosclerosis in Japanese quail was studied. The venom of Agkistrodon halys was fractionated by DEAE-cellulose chromatography and the pooled protein fractions that resulted were injected intravenously into the quail with aortic atherosclerosis induced by dietary cholesterol. After 7 weeks of injections on every other day, the quail were killed, blood clotting times and serum cholesterol levels were determined, and aortic atherosclerosis and fatty liver were scored. The results showed that while no regression of atherosclerosis was observed, the lowering of serum cholesterol, prolonged blood clotting time and reduced fatty liver were significantly affected by the injection of one of the pooled protein fractions. This venom fraction contained two major protein components, one of which had arginine esterase activity. From this study we conclude that snake venom has little effect on the regression of atherosclerosis, but it prolongs blood clotting and lowers serum cholesterol.
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PMID:Effect of snake venom of Agkistrodon halys on atherosclerosis and blood characteristics in Japanese quail. 228 93

To elucidate if the presence of fatty liver and hypertriglyceridemia (HTG) influences pancreatic A-cell function in obesity, basal and arginine-stimulated glucagon (IRG) secretions were studied in 7 normal subjects and in 28 moderately obese patients (OB) with normal glucose tolerance. The patients were divided into 4 groups, based on the presence of fatty liver and/or HTG. BMI was similar in all four obese groups. Basal IRG, as well as the sum of secretory response to arginine, namely sigma IRG values, were significantly (p less than 0.01) higher in the OB subgroup having both fatty liver and HTG than in the other three groups; these values were similar in subgroups of OB without fatty liver, and showed no significant difference from the normals. Basal and sigma IRG values in all OB correlated well with the degree of fatty liver and HTG, demonstrating that by stepwise analysis the effects of fatty liver and HTG were independent for basal and sigma IRG values. These results suggest that the combination of fatty liver and HTG may serve as a good predictor of hyperglucagonemia in simple obesity, and, hence, metabolic heterogeneity among obese patients should be considered in evaluating A-cell function.
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PMID:Elevated pancreatic glucagon in moderately obese patients: relationship of fatty liver and hypertriglyceridemia. 273 44

The prevalence of fatty liver disease at autopsy ranges from 40% to 80% in Europe and North America, and liver injury tests are abnormal in up to 8% of healthy populations. Liver injury tests were therefore examined in a group of 325 workers without exposure to hepatotoxins to identify the influence of obesity and gender. Obesity was a strong predictor of the degree of abnormality for serum levels of arginine and alanine aminotransferase and of alkaline phosphatase, even in the normal range. Women generally demonstrated lower levels of these enzymes. Workers with morbid obesity were substantially more likely to have abnormal liver injury tests. Obesity and gender must be considered in the interpretation of abnormal liver injury tests in hazardous waste workers.
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PMID:Liver injury tests in hazardous waste workers: the role of obesity. 291 8

Trifluoperazine (TFP) (50 mg/kg ip) administration to rats 6 or 10 hr after CCl4 (1 ml/kg ip in olive oil) significantly prevented liver necrosis but not fatty liver caused by the hepatotoxin at 24 hr as evidenced by either histology or electron microscopy. TFP given 6 hr after CCl4 significantly decreased the CCl4-induced increases in liver calcium content. TFP raised four to five times the liver glycogen content in control rats but was unable to modify decreased glycogen content of CCl4 poisoned animals. TFP administration increased phospholipid and protein synthesis as evidenced by studies on 32P incorporation into microsomal phospholipid and by experiments on [14C]leucine incorporation in microsomal protein fractions from control rat livers. No significant changes were observed in microsomal phospholipid degradation as studied by decay of label from 32P-prelabeled microsomal lipids or in increased protein degradation as evidenced by decay of label from [14C-guanidino]arginine-prelabeled microsomal proteins found in livers of control rats after TFP treatment. Electron microscopy observations of liver from control animals treated with TFP evidenced accumulation of glycogen in areas close to smooth endoplasmic reticulum (SER); large Golgi areas with an abundant number of lysosomes, and minor dilatation effects on the rough endoplasmic reticulum (RER) and nuclear membrane. Results suggest that TFP preventive effects might be due to the anticalmodulin actions of this drug.
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PMID:Further studies on the late preventive effects of the anticalmodulin trifluoperazine on carbon tetrachloride-induced liver necrosis. 337 54

Young rats were force-fed a lysine + arginine-devoid diet or a complete diet for 3 days, and selected biochemical and morphologic studies were conducted. Rats force-fed the experimental diet in comparison with those force-fed the control diet for 3 days showed decreased body weight gain, hepatomegaly with periportal fatty liver, pancreatic and splenic atrophy, and enhanced 14C-leucine incorporation into hepatic proteins. Differences in the experimental animals were observed in the free amino acid levels of serum (decreased lysine, arginine, and ornithine) and liver (decreased ornithine), in blood chemistries (decreased levels of ammonia N2, uric acid, cholesterol, protein, albumin, alkaline phosphatase, LDH and SGOT) and in hematologic findings (leukocytopenia and thrombocytopenia after a morning feeding). The experimental findings in young rats force-fed the lysine + arginine-devoid diet were compared with those reported to develop in children with lysinuric protein intolerance (LPI), an autosomal recessive defect in diamino acid transport. Children with LPI as described by others reveal a number of similarities as well as a number of differences in comparison to the findings in the experimental animals. The comparison suggests that some of the pathological manifestations of LPI may be related to a deficiency of diamino acids but others must be due to different alterations in this complex human disease.
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PMID:Chemical pathology of diamino acid deficiency: considerations in relation to lysinuric protein intolerance. 393 96

Weanling male Sprague-Dawley rats were fed ad libitum 15% casein diets with and without 5.0% lysine-HCI, 0.25% adenine sulfate or 0.1% allopurinol for 2 weeks. Addition of lysine alone depressed 2-week growth from 94 to 65 g increased average daily urinary orotic acid excretion from 0.39 to 1.77 mg and increased the percentage of total liver lipids from 3.6 to 11.2. Adenine or allopurinol did not change growth but markedly enhanced lysine-induced orotic aciduria and completely prevented lysine-induced fatty livers. Reports by other show that adenine and allopurinol also prevent fatty livers or rats fed arginine-free diets or excess orotic acid. The authors conclude that lysine-induced orotic aciduria results from arginine deficiency caused by antagonism of arginine function by lysine, and that lysine-induced fatty liver probably results from a lesion identical to that produced by feeding excess orotic acid.
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PMID:Fatty liver of growing rats fed excess lysine and its prevention by adenine or allopurinol. 678 27

Hepatic steatosis resulting from the consumption of an arginine-deficient diet in the rat was found to occur independent of age or size. The rate of lipid biosynthesis as indicated by in vitro incorporation of 14C-acetate was significantly increased in rats fed an arginine-deficient diet when expressed per milligram liver. Supplementation of the arginine-deficient diet with 1% ribose, 1% hypoxanthine or 0.2% adenine depressed the fatty infiltration caused by arginine deficiency. Inosine, xanthine or uracil supplementation did not significantly alter the fatty infiltration, liver orotic acid biosynthesis or urinary orotic excretion induced by the arginine deficiency. Increased orotic acid excretion was also observed in the mouse, hamster and rabbit fed a diet devoid of arginine. However, consumption of the, arginine-deficient diet for 21 days did not significantly alter the liver lipid content of mice, hamsters or rabbits. Although the fatty infiltration appears to be limited to the rat, altered liver nucleotides were observed in rats, hamsters and rabbits fed an arginine-deficient diet. Similarities of arginine deficiency and orotic acid feeding in various species are discussed.
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PMID:Species specificity of arginine deficiency-induced hepatic steatosis. 724 Dec 27

The prevalence of a mutation of the codon for tryptophan 64 to arginine (Trp64Arg) in the beta3-adrenergic receptor gene was investigated by genotyping 261 Japanese subjects. The allelic frequency of this mutation was 0.18. Subjects with the homozygous W64R mutant alleles had a significantly higher prevalence of fatty liver, BMI, serum gamma-glutamyl transpeptidase, and serum leucine amino transpeptidase levels than those without the mutation. Individuals with this mutation also showed a higher fasting blood glucose level than those without this mutation. However, the prevalence of diabetes mellitus was no different between the three groups. These results suggest a potential association of the Trp64Arg mutation with higher morbidity of fatty liver and mild glucose intolerance.
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PMID:Association of the Trp64Arg mutation of the beta3-adrenergic receptor with fatty liver and mild glucose intolerance in Japanese subjects. 969 85


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