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 purpose of this work was to study the quantitative modifications of the hepatic lipids in adult thyroidectomized rats after administration of tetracycline or ethanol (acute dose or prolonged ingestion). 1. - Thyroidectomy did not inhibit the accumulation of fat in the liver of fed euthyroid or hypothyroid rats after intraperitoneal infusion of tetracycline (320 mg/body weight in 2 injections at an interval of 16 h, the diet containing 6% of lipids). 2. - Sixteen hours after the oral administration of a single large dose of ethanol (5 g/kg body weight), there were only found some small modifications of the lipid composition of the liver in fasting euthyroid or thyroidectomized rats, receiving a diet with 6% of lipids before the experiment; on the contrary, when the diet contained 19% of lipids, a fatty liver occurred in the intact rat, but not in the thyroidectomized rat. 3. - The prolonged ethanol intake (in a 20% solution in water) for 5 months with a diet containing 19% of lipids did not induce a fatty liver in intact rats but produced a decrease of hepatic non-phosphorus lipid and an increase of the cholesterol amounts. After the administration of L-thyroxin (10 mug/100 g body weight per day) to these alcoholic thyroidectomized rats during 2 weeks, it was found an increase of the hepatic non phosphorus lipids till an higher amount than in the euthyroid rats. 4. - The hepatic phospholipid amounts were relatively constant in the different experiments. These results accounting for this differential effects were discussed.
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PMID:[Hepatic lipids of intact or thyroidectomized rats after administration of tetracycline or ethanol]. 5 33

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

Effects of dietary myo-inositol deprivation were examined during prenatal and postnatal development and during lactation in the rat. The deficient diet contained no detectable myo-inositol while the supplemented diet contained 0.5% (w/w) myo-inositol while the supplemented diet ct contained 0.5% (w/w) myo-inositol at the expense of sucrose. Both diets contained 25% casein, adequate amounts of all known vitamins, choline, and essential fatty acids as well as 0.5% (w/w) phthalylsulfathiazole to depress myo-inositol contribution to the diet by microorganisms. Pregnant rats of the Holtzman strain were fed the respective diets during gestation and lactation, and pups were fed the corresponding diet after weaning until 3 months of age. There were no significant differen-es in body weight between experimental groups. Supplementation of the diet with myo-inositol significanly increased the levels of myo-inositol in plasma, liver, kidney, and intestine of pups at all ages examined, and significantly increased the levels of myo-inositol in the milk and mammary tissue during lactation. During lactation, the myo-inositol deprived dams developed severe fatty livers (31% w/w) characterized by diminished phosphatidyl-inositol (50%) and total phospholipid phosphorus (57%) levels as compared with controls. After weaning, the liver lipid content of the myo-inositol deprived dams returned to normal (4.5%). The data suggest that a possible threshold level of free myo-inositol (approximately 0.15 mumoles/g lipid-free tissue) was required to prevent fatty liver in lactating dams under these dietary conditions. Effects of the deficient diet on fertility were also examined. Based on sperm count and production of offspring, there were no differnences between the experimental and control males. Females of both groups showed equal ability to produce offspring.
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PMID:myo-Inositol metabolism during lactation and development in the rat. The prevention of lactation-induced fatty liver by dietary myo-inositol. 97 67

The effect of two levels each of methionine (0.0 and 0.07 percent), thiouracil (0.0 and 0.05 percent), dienestrol diacetate (0.0 and 0.007 percent), and thyroactive casein (0.0 and 0.0125 percent) on the performancy, organ changes, and liver composition in 640 pullets of two strains was studied in a 24 factorial arrangement of treatments. Egg production, egg characteristics, feed conversion, organ weights, and liver composition were parameters measured. Supplemental methionine increased the phosphorus content of liver fat in strain A, but other parameters in the two strains were mot affected by the increase in dietary methionine. The thiouracil increased weight grains, gram of fat per total liver, percent of liver fat, thyroid weight, and heart weight but decreased the phosphorus content of liver fat. Nine typical cases of fatty liver syndrome with large liver hematomas occurred in the thiouracil treated birds and one case occurred in an untreated pullet. Dienestrol diacetate did not affect egg production, egg characteristics, organ weights, and liver composition in the two strains. Thyroprotein decreased weight gain, abdominal fat, liver weight. liver fat, thyroid weight, and percent red cells, but decreased percent blood sports in eggs and adjusted weights of the kidney and heart in both strains.
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PMID:The effect of methionine, thiouracil, dienestrol diacetate and thyroprotein on the development and prevention of fatty liver in pullets. 115 73

Plasma was obtained from normal laying hens, 30 weeks of age, and from laying hens, 60 weeks of age, with fatty liver syndrome (FLS). The 60-week-old hens were divided into two groups based on whether they were laying or nonlaying. Plasma phosphorus and calcium was significantly higher for hens with FLS. The younger hens had significantly lower 25-dihydroxyvitamin D3 (25-OH-D3) plasma levels than the older hens. The older hens that were laying had significantly lower 25-OH-D3 plasma levels than the nonlaying hens. Old nonlaying hens with FLS had lower 1, 25-OH-D3 than young hens or old laying hens with FLS; however, the levels were not different for the two groups of laying hens.
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PMID:Plasma calcium, phosphorus, 25-dihydroxyvitamin D3, and 1-25-dihydroxyvitamin D3 of hens with fatty liver syndrome. 383 79

The effects of late pregnancy on metabolic fuels, liver composition, gluconeogenesis, and nitrogen metabolism have been examined in fed and fasted rats. Plasma free fatty acid (FFA) and immunoreactive insulin (IRI) are greater and glucose and ketones are lower in fed 19-day pregnant than they are in agematched virgin rats. A 48 hr fast elicits greater increases in FFA and ketones and more profound reductions in glucose in the pregnant rats and obliterates the differences in IRI. Fetal weight is not modified by such fasting but maternal weight losses exceed that of the nongravid rats. Livers from rats 19 days pregnant contain more and larger hepatocytes. Per mumole hepatic deoxyribonucleic acid (DNA)-phosphorus, water and protein are more abundant, whereas glycogen is unaffected. Livers from fed pregnant rats contain more lipid phosphorus and less neutral lipid fatty acid. After a 48 hr fast, hepatic steatosis supervenes in gravid animals due to accumulated neutral fat. The contents of hepatic acetyl-coenzyme A (CoA) and citric acid are not different in fed pregnant and virgin rats but are greater in the pregnant rats after fasting. Formation of glucose-(14)C and glycogen-(14)C from administered pyruvate-(14)C are the same in fed pregnant and virgin rats, but greater in the pregnant ones after a 24 or 48 hr fast. Pregnancy does not affect creatinine excretion, and urinary urea is not different in fed pregnant, virgin, and postpartum animals. Contrariwise, more nitrogen, potassium, and phosphorus are excreted by the pregnant animals during a 2 day fast. The increment in urinary nitrogen is due largely to urea on the 1st day, whereas heightened ammonia accounts for half the increase on the 2nd and correlates with the enhanced ketonuria. Muscle catabolism, gluconeogenesis, and diversion to fat are activated more rapidly and to a greater degree when food is withheld during late gestation in the rat. These catabolic propensities are restrained in the fed state. The capacity for "accelerated starvation" may confer survival benefit upon an intermittently eating mother in the presence of a continuously feeding fetus.
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PMID:Carbohydrate metabolism in pregnancy. VI. Plasma fuels, insulin, liver composition, gluconeogenesis, and nitrogen metabolism during late gestation in the fed and fasted rat. 535 39

The content of hepatic cyclic AMP was increased soon after intoxication by white phosphorus. Its level reached a maximum 4 h after poisoning, but in subsequent phases tended to return to normal. In contrast, the cyclic GMP concentration was altered only 24 and 36 h after treatment with the same hepatotoxin. Similar modifications of cAMP and cGMP content were also detected after poisoning by trichlorobromomethane (CBrCl3). As a consequence, an altered cGMP/cAMP ratio was found in both experimental conditions. Further, the modification of cAMP content after white phosphorus was detected prior to liver damage (steatosis and necrosis), while the highest concentration of the cyclic nucleotide in CBrCl3-poisoned rats was found when fatty liver was already evident. In addition, in phosphorus-poisoned rats, the hepatic content of Ca2+ was found to be unmodified during all phases of the intoxication, while after CBrCl3 a phasic increase of the Ca2+ level was observed at 4, 24 and 36 h.
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PMID:Behaviour of cyclic nucleotides and Ca2+ levels in liver tissue of rats poisoned by white phosphorus and trichlorobromomethane. 608 12

Plasma inorganic phosphorus was determined in two experiments in hens that had fatty liver syndrome. In Experiment 1, plasma inorganic phosphorus was determined in twelve strains of hens all fed the same diet. Plasma inorganic phosphorus immediately following oviposition was elevated in all strains. The two strains in the first experiment with the highest as well as the two strains with the lowest plasma inorganic phosphorus were used in the second experiment. Each of the four strains were subdivided into three groups of 60 hens each and fed a practical layer diet containing either .30, .75, or 1.40% total phosphorus and 3.4% calcium. Significant differences were found in plasma inorganic phosphorus between strains fed the three dietary phosphorus levels. Results indicated that plasma inorganic phosphorus is related to dietary phosphorus in hens with an elevated plasma inorganic phosphorus level associated with fatty liver syndrome.
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PMID:Dietary and plasma phosphorus in hens with fatty liver syndrome. 716 26

Spatially localized 31P NMR spectroscopy was used to assay in vivo the liver of intact rats fed orotic acid (OA) in a diet which produces hepatic steatosis. Twenty-three sets of multiple volume spectra were obtained from twenty-one 265- to 315-g female rats after 0-9 days of feeding either a 1% OA/64% sucrose diet (12 rats) or a 65% sucrose control diet (9 rats). The intensity of the in vivo diphosphodiester resonance ascribed to UDP-hexos(amin)es increased and the phosphomonoester resonance decreased in intensity prior to fatty infiltration. High resolution NMR spectroscopy of extracts of these livers indicated that the UDP-hexos(amin)e peak included four different UDP-sugars including UDP-N-acetylglucosamine (UDP-glcNAc), and that lower phosphocholine (P-Cho) accounted for the lower phosphomonoester resonance in vivo. Increased UDP-glcNAc is thought to reflect impaired lipoprotein glycosylation as a mechanism for hepatic steatosis in orotic acid feeding. P-Cho deficiency has been shown to be due to an increased rate of phosphatidylcholine synthesis. Low P-Cho concentration has been shown to be associated with lipid accumulation in a choline-deficient diet, but was not previously associated with hepatic steatosis in OA feeding. Changes in phosphorus metabolites were observed 2 days prior to development of fatty liver. HPLC assay of uridine nucleotides showed a good correlation between magnetic resonance spectroscopy and HPLC quantitation. In this study there were two biochemical correlates of impaired hepatic lipid secretion detectable by in vivo assay with 31P NMR spectroscopy. This method has application for noninvasive assays in ornithine transcarbamylase-deficient patients.
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PMID:An in vivo 31P magnetic resonance spectroscopy study of uridine excess in rats fed orotic acid. 755 16

To further understand the development of fatty liver during gram-negative sepsis, we measured fatty acid uptake in addition to esterification and secretion of lipids by freshly isolated hepatocytes from fasted and fed control and Escherichia coli-treated rats. Rats were made septic by intravenous (IV) injection of 8 x 10(7) live E coli colonies per 100 g body weight. For the fasted groups, food was removed after E coli injection. Fed rats received a nutritionally adequate diet intragastrically for 5 days before and 24 hours after inducing sepsis. Twenty-four hours after E coli injection, the esterification of newly synthesized fatty acids, as measured by 3H2O incorporation, and the esterification of exogenous fatty acids, measured from 14C-palmitate incorporation, into triglyceride (TG), total cholesterol, and total phospholipid phosphorus were significantly greater in hepatocytes from fasted septic rats compared with their control rats. In fed septic rats, esterification of 14C-palmitate into TG was fourfold greater than in the fed control rats. The increased rates of esterification in hepatocytes from fasted and fed septic rats were not accompanied by an increase in the labeled TG in the medium. This inability to secrete the additional TG that the hepatocytes produce resulted in a higher concentration of cellular TG in fasted and fed septic rats than in their controls. The enzymes glycerol-3-phosphate acyltransferase (GPAT) and phosphatidate phosphohydrolase (PPH) do not appear to be factors contributing to the increased TG synthesis, since the increase in enzyme activity was not accompanied by a similar increase in TG synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulatory factors in the development of fatty infiltration of the liver during gram-negative sepsis. 820 57


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