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

We investigated the hepatocellular peroxisomes in 27 patients with steatosis of the liver by means of catalase cytochemistry, light and electron microscopic study, and morphometry. Seven normal human livers were used as controls. In our patients, fatty liver was mainly associated with alcohol abuse or obesity. Indications for a slight decrease in catalase activity and for a proliferation were found in visual evaluation of the peroxisomes. Morphometric analysis showed a significant decrease in mean peroxisomal diameter (to 87%) and a simultaneous significant elevation to numerical density of the peroxisomes (to 188%); this resulted in a normal volume density and a significant increase to (133%) in surface density. However, individual differences were found. No differences in peroxisomal characteristics were found between fatty livers of different causes. A significant inverse linear correlation between mean peroxisomal diameter and numerical density was found in patients with fatty livers. Because a similar correlation was also found when control data were added to the fatty liver data, we hypothesize that the peroxisomal compartment in human fatty livers is adapted in such a way to permit the same metabolic efficiency as in control livers.
Hepatology 1995 Sep
PMID:Alterations of peroxisomes in steatosis of the human liver: a quantitative study. 765 78

Following the pioneer report of Di Luzio (Physiologist 6, 169-173, 1963) concerning the prevention of the acute ethanol-induced fatty liver by antioxidants, many observations have shown that ethanol-induced liver injury may be linked, at least partly, to an oxidative stress resulting from increased free radical production and/or decreased antioxidant defence. The disturbances induced in the major hepatic enzymatic and non-enzymatic antioxidant systems following experimental acute and chronic ethanol administration are reviewed, emphasizing the important role of dietary alpha-tocopherol in modifying the induction of oxidative stress and its usual expression as increased lipid peroxidation. Adaptative increases in some elements of the hepatic antioxidant defence partly counteract the enhanced generation of prooxidant free radicals following chronic ethanol intake. By contrast, lipid peroxidation is favoured when ethanol is administered together with a fat-rich diet and/or various xenobiotics. Chronic ethanol feeding has also been reported to potentiate the oxidative stress resulting from an acute ethanol load. By generating potent chemoattractants for human neutrophils and/or by stimulating the expression of genes involved in collagen biosynthesis, liver lipid peroxidation may play an important role in the progression of steatosis to hepatitis and cirrhosis. Oxidative stress has been shown not to be restricted to the liver, but also to affect, under some experimental conditions of ethanol administration, extrahepatic tissues, such as the central nervous system, the heart and the testes. This stress can be partly prevented by vitamin E supplementation. Ethanol-induced antioxidant disturbances have also been reported in clinical studies in blood and liver biopsies. Pharmacological antioxidants could have beneficial effects in reducing the incidence of ethanol-induced changes in cellular lipids, proteins and nucleic acids. The antioxidants considered could act by reducing free radical production (e.g. chelators of redox-active iron derivatives), trapping free radicals themselves, interrupting the peroxidation process or reinforcing the natural antioxidant defence.
Alcohol Alcohol 1994 Sep
PMID:Alcohol and antioxidant systems. 781 35

The study investigates the effect of a singular dose of CCl4 (2.5 ml/kg) on the concentration of triacylglycerols in the liver and oxidative phosphorylation in hepatic mitochondria after 24, 72 hours, 2 and 4 weeks since CCl4 application. It was discovered that 24 and 72 hours after CCl4 application the concentration of triacylglycerols increased significantly and steatosis of the liver supervened. After 2 and 4 weeks the triacylglycerol concentration values reached the level of those of control. The hepatic steatosis disappeared. The indices of oxidative phosphorylation index of respiration control, oxygen consumption during stimulated respiration (state 3), oxygen consumption during basal respiration (state 4), and phosphorylation velocity decreased significantly after 24 and 72 hours after CCl4 application in all observed substrates--glutamate, pyruvate and jantarane. After 2 to 4 weeks the observed indices reached the level of values characteristic for healthy controls. The results have indicated that after the CCl4 toxic impairment the energy metabolism in hepatic mitochondria has been significantly impaired. This impairment, in spite of its severeness, was irreversible and hepatocytes were able to compensate it (Tab. 4, Ref. 33).
Bratisl Lek Listy 1994 Sep
PMID:[Oxidative phosphorylation in liver mitochondria after injury with carbon tetrachloride and during regeneration]. 781 46

We report the case of an otherwise healthy 11-year-old girl who died suddenly of previously undiagnosed diabetes mellitus type I, following a 2-day minor upper respiratory infection. Insulin dependent diabetes mellitus (IDDM) is a rare cause of sudden death of apparently healthy children. This report demonstrates a recommended diagnostic pathway for IDDM from the substantiation of vesicular fatty liver to specific pancreatic histological and histochemical changes.
Am J Forensic Med Pathol 1994 Sep
PMID:Sudden unexpected death in childhood due to unsuspected diabetes mellitus. 749 74

1. A total of 655 mule ducklings were produced in three hatches by artificial insemination of common duck females Brown Tsaiya and Pekin "Alienor" and of their 2 reciprocal crossbreds with Muscovy semen. 2. They were fed ad libitum until 6 weeks, then restricted to one meal per day until day 75 and afterwards preforce fed until day 84 and subsequently forced fed by 2 crammers, twice a day, from the age of 85 d and for a maximum of 13 d. 3. Body weight at hatching, 28 d, 56 d, 75 d, 84 d and at slaughter, the number of force-fed meals, the "paletot" weight, the fatty liver weight, the fat release rate after sterilisation of a 60 g portion of liver and the serous melting rate were measured individually. 4. Significant dam genotype and hatch effects were present for all traits. The crammer effect on force feeding traits was also significant. For mule ducks from Brown Tsaiya, Tsaiya x Pekin, Pekin x Tsaiya and Pekin dams respectively, mean body weight was 2356, 3219, 3137 and 3801 g at 12 weeks, "paletot" weight was 1585, 2111, 2110 and 2470 g, fatty liver weight was 441, 585, 563 and 641 g, fat release rate was 35.1, 40.5, 38.2 and 46.0%. 5. The estimated differences between Pekin and Tsaiya genetic effects in their mule progeny were significant and in favour of the Pekin, except for the number of force fed meals and for the serous melting rate.(ABSTRACT TRUNCATED AT 250 WORDS)
Br Poult Sci 1994 Sep
PMID:Genetic parameters from factorial cross breeding in two duck strains (anas platyrhynchos) Brown Tsaiya and Pekin, for growth and fatty liver traits. 782 9

1. Single comb White Leghorn hens of an inbred line highly susceptible to fatty liver haemorrhagic syndrome (FLHS) were fed supplemented dietary ascorbic acid (200 mg/kg), alpha-tocopherol (75 mg/kg), or L-cysteine (3 g/kg, and 6 g/kg) for 28 d in order to evaluate the potential therapeutic effect of these compounds against the disease. 2. Supplementation of ascorbic acid, alpha-tocopherol, or a low level of L-cysteine (3 g/kg) did not significantly affect any of the hepatic variables evaluated. Hepatic glutathione was not increased by the supplementation of dietary L-cysteine. 3. L-cysteine supplemented at a level of 6 g/kg decreased hepatic dry matter and fat contents without affecting the hepatic malondialdehyde or the liver haemorrhagic score. 4. Because one of the predisposing factors of FLHS is a high hepatic fat content it was concluded that dietary supplementation of L-cysteine (6 g/kg) may be useful in the prevention of the disease.
Br Poult Sci 1994 Sep
PMID:Effect of selected dietary antioxidants on fatty liver-haemorrhagic syndrome in laying hens. 782 18

Increased activation of lymphocytes in inflammatory bowel disease is reflected by alterations of various immunological functions including enhanced spontaneous secretion of rheumatoid factor by mononuclear cells. since in rheumatic diseases increased secretion of rheumatoid factor is associated with decreased levels of beta-endorphin in circulating blood mononuclear leukocytes, we investigated levels of leukocyte beta-endorphin in inflammatory bowel disease and compared them with those in hepatobiliary disorders and in healthy subjects. Levels of beta-endorphin were measured in extracts from peripheral blood mononuclear leukocytes by radioimmunoassay. beta-Endorphin levels ranged from 0 to 67 pg/10(6) cells. Mononuclear leukocytes from ulcerative colitis patients contained as much beta-endorphin as those from healthy control subjects. In patients with Crohn's disease, levels of beta-endorphin were reduced by as much as roughly 50%. An inverse relationship was found between leukocyte beta-endorphin on the one hand and erythrocyte sedimentation rate, blood granulocyte or thrombocyte counts, and C-reactive protein levels in plasma on the other. In patients with various hepatobiliary disorders including fatty liver disease, viral hepatitis, primary biliary cirrhosis, and cryptogenic or alcoholic cirrhosis, beta-endorphin levels were not significantly different from the normal range values. Data indicate that leukocyte beta-endorphin may be involved in regulation of the systemic inflammatory activity of Crohn's disease.
Brain Behav Immun 1994 Sep
PMID:Decreased beta-endorphin content in peripheral blood mononuclear leukocytes from patients with Crohn's disease. 786 97

Although mortality from alcoholic liver disease has declined in some Western countries in recent years, elsewhere it is increasing and overall it remains a major health problem. Deaths are predominantly seen in patients with alcoholic hepatitis or cirrhosis, and when they occur in patients with fatty liver are usually unrelated to liver disease. Progression to cirrhosis is correlated with the severity of fatty liver and particularly with the presence of alcoholic hepatitis. Mortality from cirrhosis is strongly correlated with per capita alcohol consumption. The decline in cirrhosis mortality rates seen recently is related in part to decreases in per capita consumption, but probably also to the growth of self-help organizations which facilitate abstinence from alcohol. Recent studies suggest there is not an invariable dose-response relationship between alcohol intake and the severity of liver disease and that alcohol has a permissive effect which allows other aetiological factors to operate. Factors that influence susceptibility to alcoholic liver disease include gender (women develop alcoholic cirrhosis more readily than men), concomitant hepatitis C infection and possibly hepatitis B infection. It is uncertain whether HLA status or immune mechanisms are implicated. The systematic use of screening tests for hazardous consumption combined with early intervention therapies offers a good prospect of reducing morbidity and mortality from alcoholic liver disease.
Baillieres Clin Gastroenterol 1993 Sep
PMID:Epidemiology of alcoholic liver disease. 821

In heavy drinkers with clinical evidence of liver disease, routine investigations should exclude the possibility of other chronic liver diseases of non-alcoholic aetiology requiring specific therapy--these include chronic viral hepatitis, autoimmune diseases of the liver, Wilson's disease and genetic haemochromatosis. If abnormalities in liver biochemistry persist despite abstinence, or if the diagnosis of alcoholic liver disease is in doubt, a liver biopsy should be carried out. Studies evaluating the role of liver biopsy in alcoholic liver disease suggest that without histological confirmation the diagnosis will be inaccurate in 10-20% of patients. Serum biochemistry and the currently available imaging modalities have severe limitations in determining the relative contributions of fatty liver, alcoholic hepatitis and cirrhosis to the overall picture in alcoholic liver disease. Histological examination is therefore of additional value in determining the prognosis, which is worst in patients with a combination of alcoholic hepatitis and cirrhosis. There are a number of indices available, based on clinical and laboratory information, for evaluating the short-term prognosis, but these can only be used with accuracy if the histological pattern of damage has initially been evaluated.
Baillieres Clin Gastroenterol 1993 Sep
PMID:Investigation of alcoholic liver disease. 821 5

The modulation of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) biosynthesis by sulfur-substituted fatty acid analogues has been investigated in rats. We have compared the effects of two non-beta-oxidizable fatty acid analogues, 3-thiadicarboxylic acid and tetradecylthioacetic acid, which induce proliferation of peroxisomes, with those of the analogue tetradecylthiopropionic acid, which is a weak peroxisome proliferator. Repeated administration of 3-thiadicarboxylic acid for seven days resulted in increased hepatic concentrations of both PC and PE, but the PC/PE ratio was decreased. PC synthesis was increased, as evidenced by increased incorporation of [3H]choline into PC and an increased activity of cytidinetriphosphate (CTP): phosphocholine cytidylyltransferase. This was accompanied by a reduction in the pool sizes of choline and phosphocholine. The S-adenosylmethione/S-adenosylhomocysteine ratio (AdoMet/AdoHcy) was marginally affected, indicating no increase in the rate of methylation of PE to PC. Administration of tetradecylthioacetic acid also resulted in increased hepatic phospholipid levels, increased AdoMet/AdoHcy ratios and in slightly elevated activity of CTP:phosphocholine cytidylyltransferase. The most striking effect observed after tetradecylthiopropionic acid treatment was the development of fatty liver. The activity of CTP:phosphocholine cytidylyltransferase and the incorporation of [3H]choline into PC was reduced compared to 3-thiadicarboxylic acid treatment. Although the rate of methylation of PE seemed to be increased at an elevated AdoMet/AdoHcy ratio, this resulted in only minor changes in the hepatic PC and PE levels, and the PC/PE ratio remained unchanged. Furthermore, the hepatic levels of choline and phosphocholine were reduced in these rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Lipids 1993 Sep
PMID:Modulation of phosphatidylcholine biosynthesis by peroxisome proliferating fatty acid analogues. 823 55


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