Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various aspects of lipid metabolism were examined in broiler chicks affected with fatty liver and kidney syndrome (FLKS). Plasma free fatty acid concentrations were invariably elevated. Plasma triglyceride concentrations were increased amounts of triglyceride-rich lipoproteins. Lipoprotein lipase activity in adipose tissue was considerably reduced, but in heart tissue the enzyme activity was increased. Hepatic lipogenesis was reduced. Rates of oxidation of palmitic and succinic acids by liver, heart and kidney were normal. The increased oxidation rate of palmitic acid following the addition of carnitine was also normal. These findings indicate that elevated blood lipid levels are likely to be an important factor contributing to the development of fatty deposition, particularly in extrahepatic tissues.
 ...
PMID:Some aspects of lipid metabolism in fatty liver and kidney syndrome in chicks. 16 57

cis-2-Hydroxy-2-phenyl-cyclohexanecarboxilic acid (cicloxilic acid) modifies the rat's hepatocyte intracellular movements of 3H-palmitic acid in the course of fatty liver by acute ethanol intoxication. It counteracts the impairment of radioactive lipid uptake due to ethanol treatment and promotes the early and complete release of the radioisotope inhibited by ethanol. The relevance of these results to the role of changes in the intracellular transport systems in the pathogenesis of ethanol steatosis is discussed. This and previous studies show that cicloxilic acid acts by stimulating the intracellular lipoprotein transport probably preventing by this mechanism the ethanol induced liver injury.
 ...
PMID:Influence of cicloxilic acid on the intracellular transport of 3H-palmitic acid during acute ethanol fatty liver. 58 61

Newly weaned male rats were maintained on a riboflavin-free diet for 5 weeks, and a study was made on the effect of the deficiency upon liver lipids. The content of glyceride in the livers varied among the deficient rats. High contents of glyceride were demonstrated in one-third of the deficient rats, whereas the similar level as that of control was shown in the remaining deficient rats. Contents of phospholipids and relative amounts of individual phospholipids were not altered significantly by the deficiency. Riboflavin deficiency exerted effects on fatty acid components of liver lipids. The composition of fatty acids of triglycerides varied in the deficient rats depending on the content of glycerides. However trends of increase in linoleic acid and decrease in palmitic acid towards fatty liver were observed in the deficiency in comparison with the control. On the other hand, the changes in phospholipid fatty acids were similar in all deficient rats, and the increase in linoleic acid and the decrease in arachidonic acid were brought about by the deficiency compared with controls, respectively. In liver homogenates, the incorporation of 14C-palmitate into triglycerides was higher in the deficient rats irrespective of the presence or absence of fluorde but incorporation into phospholipids was slightly lower in the deficient rats than in control animals.
 ...
PMID:Effects of riboflavin deficiency on the lipids of rat liver. 95 27

The relationship between Reye-Johnson syndrome and acute encephalopathy without fatty liver was investigated by comparing the lipid composition of liver samples obtained from five patients with Reye-Johnson syndrome, two patients with acute encephalopathy, and five controls. The mean total hepatic triglyceride concentration was increased nearly sevenfold in Reye-Johnson syndrome and slightly decreased in acute encephalopathy when compared with the mean control value. The mean total hepatic free fatty acid concentration was increased nearly threefold in acute encephalopathy when compared with the mean value in Reye-Johnson syndrome. Total phospholipid content was decreased in the liver in Reye-Johnson syndrome, and this difference was caused mainly by a diminution of the hepatic lecithin fraction. The ratio of palmitic acid to oleic acid and hepatic free fatty acids was 2.5 in Reye-Johnson syndrome, 0.7 in acute encephalopathy, and 0.8 in controls. These results suggest that, despite clinical similarities and laboratory evidence of hepatic dysfunction in both Reye-Johnson syndrome and acute encephalopathy, different pathogenic mechanisms may be responsible for the liver abnormalities found in the two syndromes.
 ...
PMID:Hepatic lipids in Reye-Johnson syndrome and in acute encephalopathy without fatty liver. 99 54

Fatty liver and kidney syndrome, a disorder of young chicks, was studied under laboratory conditions. Affected chicks had enlarged livers (hepatomegaly), an increased content of lipid in the liver, and an increased level of palmitoleic acid in the liver lipids. The disorder was observed mainly in chicks from young parent flocks, and was associated either with commerical diets which were subsequently found to be low in biotin, or with specially formulated low-biotin diets. A third factor, imposition of stress, was required to initiate the disorder. There was evidence of increased lipogenesis causing an increase of triacylglycerols in the liver lipids and an increased production of saturated fatty acids, particularly palmitic acid. Increased levels of palmitoleic acid resulted from an increased desaturation of palmitic acid. Under stress, affected chicks had low blood glucose levels, suggesting that gluconeogenesis was impaired. Since biotin-dependent enzymes are involved in both gluconeogenesis and lipogenesis, it would appear that the relevant enzymes respond differently to a deficiency of biotin.
 ...
PMID:Fatty liver and kidney syndrome in chicks. I. Effect of biotin in diet. 102 58

A micro-technique was developed to measure fatty acid oxidation in vitro and to investigate its possible derangement in alcoholic fatty liver disease. Percutaneous liver biopsy specimens were obtained from nine control subjects and 28 alcoholic patients with mild to severe fatty liver. Fresh tissue (10-15 mg) was incubated at 37 degrees C for 90 min in a sealed reaction flask containing 1.92 mmol/l [1-14C]palmitic acid (1-2 microCi) and 1% essentially fatty acid free albumin in Krebs-Henseleit buffer, pH 7.4. Radiolabelled CO2 and perchloric acid-soluble ketone bodies were isolated and counted. CO2 production was markedly reduced in alcoholic patients with mild and severe fatty liver compared with controls. This depression was reversed by the addition of malate to the reaction flask but not by carnitine or coenzyme A. Ketone body production was similar in controls and patients with mild and severe fatty liver. After the incubation in vitro, the tissue was extracted with chloroform/methanol and the triglyceride fraction isolated by thin layer chromatography and counted for radioactivity. The rate of palmitic acid incorporation into triglyceride was higher in alcoholic patients, particularly those with severe fatty infiltration, compared with controls. It is suggested that alcoholic fatty liver is accompanied by a progressive reduction in palmitic acid oxidation with the major defect occurring in the tricarboxylic acid cycle. In contrast, the rate of palmitic acid esterification into triglyceride is enhanced.
 ...
PMID:Palmitic acid oxidation and incorporation into triglyceride by needle liver biopsy specimens from control subjects and patients with alcoholic fatty liver disease. 309 34

Information regarding hepatic function during total parenteral nutrition in rats is often extrapolated to the clinical situation, but the steatosis observed in that species may simply reflect choline deficiency and be irrelevant to man. The effect of choline supplementation on hepatic lipid content and triglyceride secretion was examined in parenterally fed rats. Eighty to 90-day-old rats were randomized into three groups; group I received oral Purina Chow ad libitum, groups II and III received identical total parenteral nutrition regimens with the exception that group III received supplemental choline. After 7 days, peripheral triglyceride uptake was inhibited with Triton WR1339, the rate of secretion of 14C-labeled triglyceride measured after a bolus injection of 1-14C-palmitic acid, and total hepatic lipid content was measured. Total hepatic lipid content was elevated in group II (86.3 mg/g) and group III (83.3 mg/g), and both differed significantly from the control group I (35.2 mg/g, p less than 0.01), but the choline supplementation appeared to make no difference. Hepatic secretion of 14C-palmitic acid as 14C-triglyceride was reduced in group II (0.73%/ml plasma), and group III (0.72%/ml plasma) compared to group I (1.06%/ml plasma, p less than 0.05), and was unaffected by choline. The hepatic steatosis produced in the parenterally fed rat did not appear to be due to choline deficiency but to some other factors which may be important in man.
 ...
PMID:The effect of choline supplementation on hepatic steatosis in the parenterally fed rat. 393 Jul 66

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.
 ...
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.
 ...
PMID:Lipid metabolism in fatty liver of lysine- and threonine-deficient rats. 596 90

Hepatic steatosis frequently complicates total parenteral nutrition (TPN). Some of the mechanisms responsible were examined in rats receiving calories as dextrose (CHO-TPN) or dextrose plus lipid emulsion (Lipid-TPN). Hepatic triglyceride content increased approximately threefold after CHO-TPN and twofold after Lipid-TPN (P less than 0.02). Hepatic triglyceride fatty acid composition reflected endogenous synthesis. Hepatic acetyl-Coenzyme A carboxylase specific activity increased fourfold after CHO-TPN and twofold after Lipid-TPN, and it correlated positively with hepatic lipid content (r = 0.82). The activities of the microsomal enzymes of complex lipid synthesis were unchanged in the TPN groups. Both TPN regimens suppressed hepatic triglyceride secretion, measured by the rise in plasma triglyceride and the incorporation of [14C]palmitic acid into plasma triglyceride after intravenous Triton. Hepatic triglyceride secretion correlated negatively with total hepatic lipid content (r = -0.89). CHO-TPN increased the uptake of a radiolabeled triglyceride emulsion and increased hepatic lipase activity, whereas Lipid-TPN decreased both. Both adipose and cardiac lipase were higher for Lipid-TPN animals than for CHO-TPN or control animals. Hepatic 14C-triglyceride content was increased in both TPN groups as compared with controls after the injection of 1-[14C]-palmitic acid. This increment was proportional to the decreased hepatic secretion. Triglyceride fatty acid oxidation was significantly suppressed by CHO-TPN, less so by Lipid-TPN. Free fatty acid oxidation was suppressed only by CHO-TPN. The results suggest that the steatosis induced by TPN in rats was due to enhanced hepatic synthesis of fatty acid and reduced triglyceride secretion. Reduced hepatic triglyceride uptake, enhanced fatty acid oxidation, and enhanced peripheral tissue plasma triglyceride lipolysis when CHO-TPN is supplemented with lipid may modulate the accumulation of hepatic triglyceride and, along with reduced synthesis of fatty acid, lead to a lower hepatic triglyceride content.
 ...
PMID:Pathogenesis of hepatic steatosis in the parenterally fed rat. 643 55


1 2 3 4 5 6 7 8 9 10 Next >>