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)

Experiments were conducted from 1968 to 1974 to investigate reproductive complications and mortality in mink fed Great Lakes coho salmon and to ascertain the effects of polychlorinated biphenyls (PCB's) on this fur bearer. The results of mink feeding trials indicated that coho salmon, as such, were not responsible for the loss of reproduction in the adult, or the kit mortality. Mink diets that contained other species of Great Lakes fish caused similar reproductive complications, but to a lesser degree. Rancidity, mercury poisoning and chlorinated hydrocarbon pesticide contamination of the fish were all discounted as being responsible for the problem. The clinical signs and lesions noted in mink that died while receiving diets that contained Lake Michigan coho salmon were very similar to those observed in mink fed on rations that contained supplemental PCB's. These included anorexia, blood stools, fatty liver, kidney degeneration, and hemorrhagic gastric ulcers. Analyses of tissues from mink that died when fed 30% Lake Michigan coho salmon or 30 ppm supplemental PCB diets showed similar PCB residues. PCB toxicity experiments revealed that mink are very sensitive to these compounds and that the lethal dose varied inversely with the chlorine content of the PCB's although only Aroclor 1254 exerted a detrimental effect on reproduction when fed at a low level (2 ppm) for 8 months. The reproductive failure encountered in feeding mink Lake Michigan coho salmon and Aroclor 1254 was shown to be of a non-permanent nature.
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PMID:Current status of PCB toxicity to mink, and effect on their reproduction. 40 55

We have evaluated the 133Xenon inhalation method for the determination of splenic blood flow. In twenty-two healthy persons the blood flow was on average 109 +/- 4 mg/100 g X min, which is equivalent to a total blood flow of about 170 ml/min. In patients with chronic fatty liver hepatitis specific blood flow was reduced (81 +/- 10 ml/100 g X min) as it was in patients with cirrhotic liver without splenomegaly (75 +/- 2 ml/100 g X min). With increasing weight of the spleen, the total blood flow rises, although specific blood flow is low. Our results obtained by the 133Xenon inhalation method are similar to results obtained by others using intraarterial injection of tracer gas. The advantages of the inhalation method as a non-traumatic method are: (1) the stress for the patient is very small; (2) blood flow measurements can be repeated within short periods of time. We consider for the present the 133Xenon inhalation method to be the method of choice for the determination of the splenic blood flow.
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PMID:Determination of splenic blood flow by inhalation of radioactive rare gases. 41 64

Liver biopsy specimens were studied in 26 patients in whom liver function abnormalities developed during intravenous hyperalimentation (IVH). The clinical manifestations and duration of IVH were evaluated in relation to the morphological changes seen in the liver. Early hepatic changes consisted of fatty metamorphosis, and progressive intrahepatic cholestasis developed as IVH was continued. Essential fatty acid deficiency, amino acid imbalance, caloric excess, and toxic manifestations of certain amino acids are postulated as causative factors. The hepatic steatosis secondary to IVH may be treated by lowering the dextrose concentration of the infusion or by administering dextrose-free amino acid solutions. The clinical importance of this common complication of IVH is the difficulty in distinguishing it from other causes of cholestasis in seriously ill patients.
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PMID:Hepatic dysfunction during hyperalimentation. 41 12

It is reported on the syndrome of the acute fatty liver of pregnancy and pointed out that early diagnosis, subsequent early termination of pregnancy and intensive treatment of complications, especially of hepatic and renal failure and disturbed blood clotting could reduce the mortality from almost 90 to 45 per cent within the recent years.
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PMID:[The syndrome of acute fatty liver in pregnancy]. 42 6

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

In 7 obese patients with an overweight of 53 +/- 19% of Broca we found a 2-fold enlarged apparent volume of distribution and a nearly 2-fold prolonged elimination halflife of hexobarbital; the hexobarbital plasma clearance however, which is nearly identical with the metabolizing capacity of the liver for hexobarbital, was not decreased. Phenobarbital induced the microsomal drugmetabolizing enzyme system in the fatty liver of genetically obese mice in the same way 2-3-fold as in the non-fatty liver of the lean littermates.
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PMID:[Studies on drug metabolism in obese men and mice (author's transl)]. 43 68

Ninteen cases of radiographically visible fatty liver are presented. The four radiographic signs are muscle-fat interface, fat-water interface, a visible hollow viscus wall, and blurring of the medial margin of the right properitoneal fat stripe. The last sign, the authors believe, is the earliest radiographic change in developing fatty liver. In one case, isolated glycogen synthetase deficiency was the cause of fatty liver; this finding, to the authors' knowledge, has not previously been described. The value of the chest radiograph in diagnosing fatty liver is stressed.
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PMID:The radiographic signs of fatty liver. 44 17

Sampling variability of liver biopsy was determined in three consecutive biopsy specimens obtained from each of 118 patients immediately prior to autopsy. No sampling variability was found for fatty liver, alcoholic hepatitis, nonspecific hepatitis, fulminant hepatitis, leukemic infiltrate, and venous congestion. Cirrhosis was diagnosed in 80% of cases at the first biopsy but in all cases after three biopsies. Chronic aggressive and chronic persistent hepatitis were diagnosed correctly in two of three cases each at the first biopsy, and in all cases after three biopsies. Metastatic carcinoma was detected in 46% of cases at the first biopsy and in 69% after three biopsies. Granulomas were missed once on the first biopsy, but found on a subsequent biopsy. The amounts of fat and fibrosis in the biopsy specimens often were not representative of the amounts present at autopsy.
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PMID:Sampling variability on percutaneous liver biopsy. 44 70

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

The time-course of plasma lipid alterations and of triglyceride accumulation in the liver was investigated in male and female rats 12, 24 and 48 hours after treatment with 3.48 mmole/kg (0.75 g/kg) D-galactosamine (Ga1N). In the early stages of Ga1N-induced liver injury the concentrations of triglycerides, phospholipids and total cholesterol decreased, while in the later stages these values in the plasma increased above normal, especially in male animals. In contrast, glucose concentrations continually decreased, while free fatty acid (FFA) levels rose to twice those normal in female animals. Male animals had significantly lower FFA-values throughout the experiment. Consistently, the triglyceride accumulation on liver was 75 mg/g in female animals 24 hours after Ga1N administration, while male animals in the average showed only 33 mg/g triglycerides. Similar fatty infiltrations were obtained in female animals with the rather low doses of 1.16 and 2.32 mmol/kg Ga1N. It is concluded that the increase of FFA-influx after Ga1N administration is the main cause for fatty infiltration, the sex differences in the plasma FFA concentrations explaining the net differences in liver triglyceride accumulation. Additional effects in the pathogenesis of fatty liver might stem from disturbed glycosylation reactions and/or an altered secretion and metabolism of lipoproteins after Ga1N-induced liver injury.
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PMID:Liver injury and lipid metabolism: sex differences in the fatty liver induced by d-galactosamine. 46 86


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