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)

Treatment of rats with allylisopropylacetamide results in two related effects that occur sequentially. After one injection, serum FFA concentration increases and fatty liver develops without any decrease in lipoprotein synthesis. With repeated administration of the drug, fatty acid mobilization continues and acetate incorporation into lipids increases. However, fatty liver disappears with a concomitant increase in lipoprotein synthesis, resulting in hyperlipemia. It is postulated that accumulation of the liver lipid might be a regulating factor in the synthesis and transport of lipoproteins.
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PMID:Mechanism of fatty liver development and hyperlipemia in rats treated with allylisopropylacetamide. 554 7

The effects on lipid metabolism of long-term feeding of large amounts of ethanol or glucose differed from those that have been reported in short-term experiments. Three groups of male rats were investigated. The first was fed lab chow and 15% (v/v) ethanol ad lib.; the second was pair-fed with the first and given isocaloric amounts of glucose in lieu of ethanol; the third was fed lab chow and water ad lib. All three groups consumed nearly the same number of calories, and about 30% of the calories in the first group were derived from ethanol. Neither glucose nor ethanol added to a nutritionally adequate diet promoted the development of a fatty liver, although both stimulated acetate-(14)C utilization for hepatic lipid synthesis. In all three groups more than 80% of the label in hepatic lipid was found in fatty acids, and the distribution of label amongst the fatty acids of different chain lengths was virtually the same. Ethanol decreased while glucose increased the quantity of lipid in fat depots, and each altered the fatty acid composition of the lipids in adipose tissue, kidney, liver, and hepatic subcellular fractions in a different manner. The most striking of these changes was the relative increase in monounsaturated fatty acids and the decrease in essential fatty acids produced by glucose.
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PMID:Effects of prolonged ingestion of glucose or ethanol on tissue lipid composition and lipid biosynthesis in rat. 594 32

Rats were fed a low protein diet deficient in and supplemented with lysine and threonine. Liver lipids contained more lecithin, sphingomyelin, and free fatty acids, and less amino phospholipids in the deficient rats. No variations in fatty acid composition of choline- and ethanolamine-containing phospholipids were found; only palmitic acid was increased in the serine-containing phospholipids of the deficient animals. The incorporation of acetate-(14)C into phospholipids, but not into other liver lipids, was lower in deficient rats. In the plasma of deficient rats the concentration of esterified fatty acids and phospholipids was lower, of free fatty acids higher, than in the controls. The fatty acid composition of depot fat differed from that of liver neutral fat both in deficient and supplemented animals. The results presented establish that multiple metabolic defects resulting from lysine and threonine deficiency accompany the fatty liver. The design of the experiments does not permit conclusions to be drawn regarding the causal relationship between the various alterations in lipid metabolism and the fatty liver.
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PMID:Lipid metabolism in fatty liver of lysine- and threonine-deficient rats. 596 90

The role of glucose-6-phosphatase (G6Pase) in postreceptional glucose handling in non-insulin dependent diabetics ( NIDDs ) was in investigated by comparing the enzyme values in diagnostic liver biopsy samples with fasting blood glucose (BG), immunoreactive insulin (IRI) and plasma antipyrine half-life (T/2). The NIDDs , treated with sulphonylureas, had elevated serum aminotransferase and alkaline phosphatase values associated with fatty liver with or without fibrosis. G6Pase activity was reduced in the NIDDs compared with subjects who had undergone gallstone surgery (p less than 0.001), insulin dependent diabetics (p less than 0.001), and age- and sex-matched non-diabetics (p less than 0.001). G6Pase was inversely related to BG and antipyrine T/2, but not to IRI or conventional liver function tests. Therapy with phenobarbital and medroxyprogesterone acetate, known inducers, increased G6Pase activity, shortened antipyrine T/2, reduced BG and did not alter IRI, in four NIDDs . Low liver G6Pase activity in NIDDs may hence be one factor underlying the impaired glycemic control.
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PMID:Hepatic glucose-6-phosphatase activity in non-insulin dependent diabetics. Effect of enzyme-inducing drugs. 632 98

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

Alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), and P450IIE1 are the primary enzymes that catalyze the conversion of ethanol to acetaldehyde and then to acetate. Genetic polymorphisms have been reported in ADH2, ADH3, ALDH2, and the 5'-flanking region of P450IIEI. In this study, we used multivariate analysis to determine which genetic polymorphisms in alcohol metabolizing enzymes were independently associated with the development of alcoholic cirrhosis. Thirty-four noncirrhotic alcoholic patients, including 27 with fatty liver and 7 with nonspecific changes, and 46 patients with alcoholic liver cirrhosis were studied. Restriction fragment length polymorphisms (RFLPs) in the ADH2 and P450IIE1 genes were detected by digestion of polymerase chain reaction (PCR)-amplified DNA with MaeIII and RsaI, respectively. In the ALDH2 gene, RFLPs were detected by differences in the MboII site after PCR amplification. By multivariate analysis of four significant factors including total alcohol intake, ADH, ALDH, and P450IIE1 using the multiple logistic regression model, genotype ADH2(2)/ADH2(2) (P = .029) and genotype c1/c1 of P450IIE1 (P = .013) were found to be independently associated with alcoholic cirrhosis. The odds ratios for ADH2(2)/ADH2(2) genotype and the type A genotype of P450IIE1 (c1/c1) were 4.600 and 4.006, respectively. These results suggest that ADH2 and P450IIE1 gene polymorphisms may be independently associated with the development of alcoholic liver cirrhosis in Japan.
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PMID:Polymorphisms in alcohol metabolizing enzyme genes and alcoholic cirrhosis in Japanese patients: a multivariate analysis. 870 76

Protein kinase C (PKC) activity was evaluated and the phosphorylation of its endogenous substrates was explored in fatty liver induced by administration of ethionine (an analogue of methionine) to cows in order to assess the relevance of PKC-dependent phosphorylation in the development of fatty liver. PKC activity was decreased in both the cytosolic and the total particulate fractions from fatty livers, compared to the corresponding fractions from control liver. The mode of activation by the PKC cofactors (1-oleoyl-2-acetyl-sn-glycerol, 12-O-tetradecanoylphorbol-13-acetate, phosphatidyl-serine and Ca2+) was similar in both control and fatty livers, suggesting a quantitative but not a qualitative change in PKC in fatty liver. At least three substrate proteins (34 kDa, 26 kDa and 19 kDa) were found in the cytosolic fraction and their phosphorylation was reduced in fatty liver. These results suggest that impairment of the signal transduction pathway mediated by PKC is involved in the pathogenesis of fatty liver in cows.
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PMID:Reduced protein kinase C activity and endogenous protein phosphorylation in ethionine-induced fatty liver in cows. 770 79

Thus far, a large number of hypothesis have been proposed to explain how ethanol causes liver diseases including fatty liver, hepatitis, hepatic fibrosis, cirrhosis, as well as hepatocellular carcinoma. Although it still remains obscure, recent progress of science enables us to understand the mechanisms more deeply. We reviewed the latest aspects of mechanisms of alcoholic liver diseases, including alteration of redox state, effects of acetaldehyde and acetate, changes of metabolisms of lipid and protein, production of free radicals, alteration of hepatic micro circulation, change of hepatic membrane composition followed by changes of intracellular signal transduction, and effects of endotoxin. Moreover, we discussed the recent progress of studies on enzyme systems which participate in ethanol metabolism.
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PMID:[Recent progression in research on alcoholic liver disease]. 904 44

Our preceding paper reported that mepanipyrim, a new fungicide, induced fatty liver in the rat. This study was undertaken to examine this phenomenon further on hepatic triglyceride (TG) synthesis, on liver and serum lipid concentrations, and on concentration of serum very-low-density lipoprotein (VLDL) in rats fed for 3 weeks on the drug at 4,000 ppm. Mepanipyrim decreased the incorporation of 14C-acetate into hepatic TG, total cholesterol (TC) and total lipids. In addition, mepanipyrim treatment induced a drastic increase in hepatic TG accompanying a decrease in serum TG. Esterified cholesterol (CE), phospholipid (PL) and non-esterified fatty acid (NEFA) also increased in the liver with a concomitant decrease in the serum. The decrease of serum VLDL by mepanipyrim was comparable to the decrease in serum TG. Because hepatic TG is secreted into the blood by forming VLDL, which consists of TG, TC, PL, and apoprotein, the decrease in serum TG would be mainly ascribable to that in serum VLDL. Mepanipyrim also decreased serum concentrations of low-density lipoprotein (LDL) and high-density lipoprotein (HDL), and the relative weights of the epididymal adipose tissue, indicating that a reduction in serum VLDL does not reflect acceleration of serum VLDL dissimulation. These results suggest that the fatty liver induced by mepanipyrim would be due to the inhibition of hepatic VLDL synthesis or its secretion into the blood.
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PMID:Effects of mepanipyrim on lipid metabolism in rats. 977 16

Preventive effects of dehydroepiandrosteone acetate (DHEA-A) and clofibrate (positive control substance) on the fatty liver induced by orotic acid (OA) were examined on the male Sprague-Dawley rats fed a high sucrose based diet containing 1% OA and this diet further mixed with 0.5% DHEA-A or 0.5% clofibrate for 2 weeks. Numerous lipid droplets were observed in the hepatocytes of the rats treated with OA alone, but not in those treated with DHEA-A or clofibrate. In comparison to the group with OA alone, the DHEA-A or clofibrate treated rats showed a larger relative liver weight (to body weight) which was accompanied by increased peroxisomes in the hepatocytes. These results indicate that DHEA-A, as well as clofibrate, may prevent OA-induced fatty liver.
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PMID:Preventive effects of dehydroepiandrosterone acetate on the fatty liver induced by orotic acid in male rats. 1006 69


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