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

1 A series of experiments were conducted to investigate the effects of dietary retinol status on chickens ingesting aflatoxin B1. The effects of dietary supplementation with biotin and alpha-tocopherol were also examined. 2. Aflatoxin B1 levels greater than 1 mg/kg diet had a detrimental effect on 'liveability', body-weight gain, food intake and food conversion efficiency. When fed for more than 2 weeks aflatoxin increased relative liver weight and liver lipid concentration. These effects were less pronounced with avitaminotic A chickens. 3. A synergistic effect on hydropericardium development was observed between aflatoxin B1 and retinol. This effect was not observed when the dietary level of alpha-tocopherol was increased tenfold. 4. The specific activities of certain hepatic lipogenic and amino acid-metabolizing enzymes were influenced by aflatoxin ingestion. A reduction in lipogenic enzyme activity was observed before a reduction in the activities of amino acid-metabolizing enzymes. 5. Liver fatty acid composition was significantly influenced by aflatoxin B1. The extent of these changes was reduced by the inclusion of additional dietary biotin.
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PMID:The influence of vitamin A status on the response of chickens to aflatoxin B1 and changes in liver lipid metabolism associated with aflatoxicosis. 46 42

Glutamate oxaloacetate transminase (GOT), glutamate dehydrogenase (GDH), sorbitol dehydrogenase (SDH), pseudo-cholinesterase (ChE) and various blood constituents were measured in the plasma of Japanese quail fed 1,1-di(p-chlorophenyl)-2-chloroethylene (DDMU) at low levels for periods ranging from 2 to 32 days. Previous work has shown that DDMU is a potent inducer of hepatic microsomal enzymes causing marked structural changes in the liver. A rapid increase in plasma GOT was observed within 4 days accompanied by an increase in relative liver weight. Plasma GDH and SDH increased to a maximum between 16 and 24 dyas which seems to be associated with hepatic cell proliferation. Plasma ChE showed a steady increase over the time course of DDMU administration. The level of plasma lipid was reduced after 4 days whereas the hepatic lipid content was substantially increased suggesting that the fatty liver condition may be caused by decreased release of triglyceride from the liver. Plasma glucose was reduced at 8 days but there was no evidence of a hyperglycaemic state. The changes noted after 2 days of DDMU diet were confirmed by measurements on birds 18 h after oral dosing the DDMU. The study demonstrates the value of plasma enzyme measurements for the early detection of toxic effects and indicates that DDMU administration leads to extrahepatic effects in addition to those previously described in the liver.
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PMID:The effects of 1,1-di(p-chlorophenyl)-2-chloroethylene on plasma enzymes and blood constituents in the Japanese quail. 46 32

Chronic hepatitis is one of liver diseases with arguments from the clinical and histopathological aspects. Histopathological examinations were made on 687 biopsy cases clinically diagnosed as chronic hepatitis. Histopathological classification was based on our own criteria by referring to discussions in the series of Inuyama symposia on hepattis and others. The correlation between histological diagnosis and clinical data was also examined. Histopathological diagnoses made of the 687 cases were classified as follows; normal liver or liver with no pathognomonic changes of 77 cases (11.2%), non-specific reactive hepatitis of 56 cases (8.0%), viral hepatitis of 488 cases (71.0%), alcoholic hepatitis of 25 cases (3.6%), fatty liver of 23 cases (3.3%), massive liver necrosis of 3 cases, liver fibrosis of 2 cases, congestive liver of 1 case, and unclassified 12 cases due to inadequate specimens or other reasons. Among 488 viral hepatitis cases, histological stages were as follows; acute hepatitis (38 cases, 7.8%), persistent hepatitis (23 cases, 4.7%), chronic inactive hepatitis (142 cases, 29.1%), chronic active hepatitis (165 cases, 33.8%), chronic hepatitis with subloblar necrosis (33 cases, 6.8%), precirrhosis (51 cases, 10.5%), cirrhosis (27 cases, 5.5%). The relationship between histological aspects and clinical features was discussed by sex, age, and others. Of 41 follow up cases, significant values of histological type, presence of HB ag., or alcoholic were discussed as for the causative factors evolving liver cirrhosis.
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PMID:[Chronic hepatitis--clinicopathological studies of 687 cases (author's transl)]. 46 98

Two patients presenting with acute fatty liver of pregnancy were studied. Because of similarities between acute fatty liver of pregnancy and Reye's syndrome, we investigated hepatic ultrastructure, urea-cycle enzyme activities, and plasma amino acids. Initial liver biopsies obtained 12 and 21 days after the onset of illness demonstrated microvesicular fat deposition and mitochondrial ultrastructural changes, including pleomorphism and abundant crystalline inclusions. In both biopsies, activity of the mitochondrial urea-cycle enzyme OTC was markedly below normal limits. Activity of the other mitochondrial urea-cycle enzyme, CPS, was low in one patient. Abnormalities of these enzymes persisted in second biopsies obtained at 9 and 28 weeks, respectively. By 44 weeks all urea-cycle enzyme activities had returned to normal in one patient. However, in the other patient OTC activity was still reduced at 52 weeks, although it had doubled in comparison to previous biopsies. Morphological changes of the mitochondria generally improved in parallel with the urea-cycle enzymes. Plasma amino acids, obtained at the time of the initial biopsies, demonstrated a generalized hypoaminoacidemia with the exception of glutamate. Serial observations in patients with this rare disease indicate that there are similarities with Reye's syndrome, in particular, reduced activity of the mitochondrial urea-cycle enzymes. But there are important differences. (1) Enzymatic and ultrastructural abnormalities of mitochondria persist for a longer period of time than in Reye's syndrome. (2) Mitochondrial ultrastructure is different. (3) Plasma amino acid profiles are different.
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PMID:Abnormalities of hepatic mitochondrial urea-cycle enzyme activities and hepatic ultrastructure in acute fatty liver of pregnancy. 46 76

There are two metabolic disorders of major commercial importance in poultry that involve the occurrence of fatty deposits in the liver. Fatty Liver and Kidney Syndrome (FLKS) affects young birds and the main manifestations, lipid infiltrations into liver and many other organs, are apparently secondary effects of the primary lesion that lies in carbohydrate metabolism. Although several nutritional and environmental factors influence FLKS, the main factor is the vitamin, biotin. In the absence of an adequate supply of biotin, the hepatic activity of pyruvate carboxylase, a biotin-dependent enzyme, becomes so low that gluconeogenesis in the liver via pyruvate becomes negligible. When the bird is then subject to a mild stress and/or short term fasting, liver glycogen reserves become rapidly depleted and a progressive hypoglycaemia develops that ultimatley proves fatal. Supplementing diets with adequate amounts of biotin can prevent the syndrome. Fatty Liver Haemorrhagic Syndrome (FLHS) is brought about by an excessive accumulation of fat in the livers of adult hens which weakens the cellular structure of the liver and allows fatal haemorrhaging to occur. The aetiology of the syndrome is not clear, but a major factor is an excessive intake of dietary energy. However, the involvement of hormonal and toxicological factors, as well as other nutritional factors, is also possible.
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PMID:Nutritional and metabolic aspects of fatty liver disease in poultry. 47 52

Reye's syndrome (encephalopathy and fatty liver) is generally considered a disease of children. Four patients, aged 16, 18, 19, and 23 years, with Reye's syndrome were initially seen by internists. A viral prodrome followed by vomiting and encephalopathy without focal neurological signs or jaundice clinically suggested Reye's syndrome. Normal findings of CSF examination (except for increased opening pressure), abnormal findings of liver function tests, and increased blood ammonia further supported the diagnosis. None was hypoglycemic. Reye's syndrome was related to influenza B virus in three patients and to Varicella in another. Three patients survived. Reye's syndrome may be seen intially by general practitioners, emergency room physicians, internists, or psychiatrists. The importance of considering this syndrome in the differential diagnosis of unexplained encephalopathy in adults is stressed.
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PMID:Reye's syndrome in nonpediatric age groups. 48 May 58

Acute hydrazine exposure elevated rat liver triacylglycerol content and produced a rapid rise in triacylglycerol production from sn-[1,3-14C]glycerol 3-phosphate by liver homogenate and microsomal fractions. Hydrazine treatment also increased the incorporation of [1,3-14C]glycerol into hepatic triacylglycerol by the intact animal. Homogenates of hepatocyte monolayers exposed to hydrazine in vitro also exhibited an increased capacity to form triacylglycerol from sn-[1,3-14C]glycerol 3-phosphate. Hydrazine-dependent increases in hepatic triacylglycerol production measured in vitro correlated well with an increase in microsomal phosphatidate phosphohydrolase (EC 3.1.3.4) activity. Therefore, the fatty liver associated with hydrazine exposure may be explained in part by a rise in the enzymatic capacity of hepatic triacylglycerol biosynthesis.
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PMID:Effect of hydrazine exposure on hepatic triacylglycerol biosynthesis. 48 20

Collagenisation of the space of Disse was systematically assessed to determine its relationship to the clinical and histological manifestations of chronic alcoholic liver disease. Ninety-four chronic alcoholics who had been submitted to biopsy were assessed by clinical manifestations of hepatic dysfunction and by a 17-parameter Combined Clinical and Laboratory Index (CCLI). Liver biopsies were scored for light (LM) and electron-microscopy (EM) abnormalities using a universal scoring system for both. Thirty-five patients with normal liver histology (LM) had an average collagen score of 0.6 +/- 0.1. Twelve cirrhotic patients and 29 with fatty liver, both groups with mild clinical manifestations, did not differ significantly. In 18 cirrhotic patients and five with fatty liver, both groups having severe clinical manifestations, the mean scores were 2.1 +/- 0.8 (P less than 0.02) and 2.5 +/- 0.6 (P less than 0.01) respectively. Collagenisation also correlated with CCLI (P less than 0.001), serum bilirubin (P less than 0.001), serum aspartate transferase (SGOT) (P less than 0.003), and clinical evidence of portal hypertension and histological changes of necrosis, inflammation, and terminal hepatic vein sclerosis. These results suggest that collagenisation of the Disse space may be important in the pathogenesis of alcoholic liver disease.
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PMID:Collagenisation of the Disse space in alcoholic liver disease. 48 62

Lysosome are subcellular particles in which several acid hydrolases of various specificities are localized. The role of lysosome in cellular physiology and pathology has drawn considerable recent attention by several groups of investigators. The purpose of this study was to investigate the activities of lysosomal enzymes--acid phosphatase, beta-glucuronidase, N-acetyl-beta-glucosaminidase--in hepatic disorders. 1) The serum levels of beta-glucuronidase and N-acetyl-beta-glucosaminidase were significantly elevated in patients with diseases of the hepatobiliary system. 2) N-acetyl-beta-glucosaminidase activity in urine specimens from patients with diseases of the hepatobiliary system was found to be significantly higher than in urine specimens from normal adults. 3) Male albino rats of 150 approximately 200 g body weight were used. CCl4 was injected intraperitoneally (dose 0.1 ml of CCl4 per 100 g body weight twice a week for eight weeks). The free activities of lysosomal enzyme were increased and high free/total activity ratios were found in the liver lysosomal fraction of CCl4 intoxicated rats. The results of these experiment indicated that the membranes of lysosome were more permeable to their enzymes, and the release of these enzymes were found in the experimental fatty liver by CCl4. 4) Corticosteroids and chloroquine stabilized rat liver lysosome in vitro from the labilizing influence of incubation at 37 degrees C. 5) The administration of chloroquine to CCl4 intoxicated rats did not cause any well-expressed stabilization of lysosomes. 6) When alpha-Tocopherol was administrated to CCl4 intoxicated rats, the decrease of bound activity and increase of free activity in lysosomal fraction, and increase of acid hydrolases, GOT and GPT in serum were inhibited.
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PMID:[Studies on lysosomes in hepatic disorders (author's transl)]. 48

From a group of 424 patients with histologically verified fatty liver 92 patients without diabetes mellitus and alcohol abuse were subjected to follow-up examination for 3 1/2 years. 56 patients underwent second liver biopsy at this time; 20 of these patients had shown marked fatty liver at the initial liver biopsy examination. These 20 patients with marked fatty liver and 25 further patients with moderarte fatty liver could be followed up 5 and 7 1/2 years later; the clinical examination, the various liver function tests, liver scan and blind liver biopsy did not show any evidence of progression of fatty liver towards chronic inflammatory liver disorders or precirrhotic states. This clinical study therefore suggests the harmlessness of non-alcoholic fatty liver.
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PMID:Follow-up study on patients with non-alcoholic and non-diabetic fatty liver. 49 27


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