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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Efficiency of protein utilization and lysine metabolism were studied in growing rats of the Zucker 13M strain, both obese and lean, and in the Charles River CD strain. When graded levels of wheat gluten or wheat gluten supplemented with lysine were fed to these three types of rats, no significant differences in the efficiency of protein utilization were found. However, under these dietary conditions, the Zucker obese rats appeared to be about 167% more efficient in energy utilization than the Zucker lean rats or the Charles River strain. The response of liver lysine-ketoglutarate reductase to the dietary treatment was similar in these three types of growing rats. The enzyme activity was induced by dietary lysine. Rats fed a lysine-deficient purified diet had a significantly lower enzyme activity than those fed a protein-free diet indicating that the same adaptive mechanism for lysine conservation as previously observed in adult rats also occurred in the growing animal. Interaction between dietary and genetic factors on fatty liver was found in this study. The most severe fatty liver was observed in the Zucker obese rats fed the most lysine-deficient diet containing 8% wheat gluten protein.
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PMID:Protein utilization and lysine metabolism in obese and non-obese growing rats. 63 44

Two experiments were conducted with White Leghorn laying hens to study the effects of different cereal grains on production criteria and liver fat content. The results of Experiment 1, in which pullets 21 weeks of age were used for a period of 22 weeks indicated that Gaines wheat or triticale (Trailblazer) were equal to corn in supporting egg production, egg weight and body weight, with comparable feed consumption. Henry wheat(a hard red winter class) was slightly, yet significantly (P less than 0.05) inferior to corn for the above criteria. No significant differences were observed among four treatments in wet liver weight and liver fat content. Hens fed the corn diet had significantly (P less than 0.05) lower carcass fat followed by the hens fed triticale in comparison with those fed Gaines or Henyry wheat. Mortality was very low and not related to dietary treatments. Neither dietary fat nor energy content was related to fat content of liver and carcass of the hens. Body weight and liver fat content were not closely related to each other. Wet liver weight was the only significantly (P less than 0.05) related factor to liver fat content. In the second experiment, in which hens 33 weeks of age were used for an experimental period of 20 weeks, opaque-2 corn was slightly superior to normal corn and triticale was comparable to normal corn in supporting egg production and egg weight. Supplementation of the diets containing the two corns and triticale with lysine failed to improve egg production and egg weight. Hens fed the diets containing either normal corn or opaque-2 corn as the only grain in the diet had significantly (P less than 0.05) higher liver fat content in comparison with hens fed the diet containing triticale as the only grain. Mortality, however, was much higher among hens fed triticale-containing diets in comparison with groups fed corn-containing diets in spite of the fact that they had significantly lower liver fat content. Regardless of dietary treatments or grains used, the hens that died were diagnosed to have fatty liver hemorrhagic syndrome. Dietary fat content was postively and significantly (P less than 0.05) related to liver fat content. Dietary energy or body weight was not closely related to liver content. Liver fat content and mortality were negatively related to each other. The higher for content did not adversely affect laying performance.
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PMID:Effects of different cereal grains in diets for laying hens on production parameters and liver fat content. 94 67

Male weanling rats were fed a 72% rice diet containing no detectable carnitine and limiting in threonine and lysine. Such dietary conditions may simulate protein malnutrition in man. Under these conditions growth impairment, anemia, hypoproteinemia, and fatty liver developed. The study focused principally on the fatty liver syndrome which was corrected to varying extents depending on degrees of supplementation with carnitine, lysine, threonine, and appropriate combinations of these nutrients. Such reduction in fatty liver accumulation was accounted for principally by the lowering of triglycerides, but also in part of total cholesterol levels. All the data, which also included monitoring carnitine uptake by the tissues and measurement of plasma triglycerides, were consistent with the view that fatty liver accumulation occurs in amino acid deficient diets because (a) of an impairment in the synthesis of the lipoprotein complex mandatory for triglyceride secretion from the liver and (b) from a deficiency of carnitine needed for the intramitochondrial transport of fatty acids prerequisite for their oxidation.
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PMID:Dietary lysine and carnitine: relation to growth and fatty livers in rats. 124 84

The amino acid composition of proteins from liver mitochondrial membranes has been studied in patients with normal liver, with biliary diseases and fatty liver, with obstructive jaundice or liver cirrhosis. A characteristic pattern of the amino acid composition in patients with normal liver has been found. In the mitochondrial membranes of patients with fatty liver tryptophan and lysine were decreased while [aspartic acid plus asparagine] and [glutamic acid plus glutamine] were increased compared to their counterpart in the normal liver. In patients with obstructive jaundice of short duration (less than two months) only a slight decrease in methionine content was found, while in the case of liver cirrhosis amino acid composition was markedly changed.
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PMID:Amino acid composition of human liver mitochondrial membranes in normal and pathological conditions. 186 76

Female NMRI mice were fed diets containing l-ethionine (0.1 and 0.3% w/w) and phenylalanine (3% w/w), as well as respective control diets. Ethionine, the S-ethylated analog of methionine, was shown to inhibit phenylalanine hydroxylase in vivo, whereby in vitro kinetics remained unaffected. Treatment with ethionine resulted in fatty liver, reduced ATP content of liver, and alterations in serum amino acid concentrations. In the high dosage ethionine group, for instance, concentrations of Ala, Gly, Ser, Met, and Phe were increased whereas concentrations of Lys, Asp, and Pro were decreased. Applying ethionine together with phenylalanine resulted in hyperphenylalaninemia and phenylketonuria. Feeding phenylalanine alone also led to decreased activity of phenylalanine hydroxylase and increased concentration of Phe in serum. Ethionine only had a minimal effect on body weight gain; however, the hyperphenylalaninemic condition induced by application of the high dosage of ethionine and phenylalanine induced severe loss of body weight. A disturbed protein synthesis and protein phosphorylation might be the underlying mechanism of ethionine-induced suppression of phenylalanine hydroxylase.
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PMID:Induction of hyperphenylalaninemia in mice by ethionine and phenylalanine. 374 96

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

In rats, chronic ethanol feeding was found to enhance the postprandial hyperlipemia and to increase the incorporation of dietary palmitic acid-(3)H and intravenously injected L-lysine-(14)C into serum lipoproteins. The main increases of total amount, labeling, and specific activity of lipid and protein occurred in the d < 1.019 lipoprotein fraction. Fat absorption and the clearance of injected chylomicrons were not affected by ethanol feeding. Blocking of lipoprotein and chylomicron removal with Triton did not prevent the action of ethanol on serum lipids, indicating that the ethanol effect is not likely due to defective removal of lipids from the circulation. Ethanol enhanced the incorporation of chylomicron fatty acids into newly synthetized very low density lipoproteins, as shown by an increased reappearance of the fatty acid label into the lipids of this fraction after injection of palmitate-(14)C/glycerol-(3)H doubly labeled chylomicrons. These results indicate that alcoholic hyperlipemia is due, at least in part, to an increase in newly synthetized lipoproteins. The hyperlipemia produced by ethanol was accompanied by hepatic steatosis. The simultaneous production of fatty liver and hyperlipemia makes it unlikely that defective lipoprotein synthesis or secretion is a primary mechanism for the pathogenesis of the alcoholic fatty liver.
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PMID:Efcts of chronic ethanol feeding on serum lipoprotein metabolism in the rat. 544 77

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 lipid-lowering effect of carnitine and its precursors, namely lysine plus methionine, was examined in male Sprague-Dawley rats fed ethanol as 36% of the total calories. Ethanol caused typical hepatic steatosis characterized by significant accumulation of total lipids, triglycerides, cholesterols, phospholipids, and free fatty acids. Supplementation of the ethanol diet with 1% DL-carnitine, 0.5% L-lysine, and 0.2% L-methionine significantly lowered ethanol-induced increases of various lipid fractions, with the exception of free fatty acids. The lipid-lowering effect of carnitine was superior to that of its precursors and their effect together was no greater than that of carnitine alone. The triglyceride contents of liver and plasma were related inversely to the levels of carnitine and acyl carnitines. It is concluded that dietary carnitine more effectively than its precursors prevented alcohol-induced hyperlipemia and accumulation of fat in livers. Thus, a deficiency of functional carnitine may indeed exist in chronic alcoholic cases.
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PMID:Ameliorating effects of carnitine and its precursors on alcohol-induced fatty liver. 642 29

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


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