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

The role of biotin-dependent enzymes in the fatty liver and kidney syndrome of young chicks was studied. Under conditions of a marginal deficiency of dietary biotin, the level of biotin in the liver has differing effects on the activities of two biotin-dependent enzymes, pyruvate carboxylase and acetyl-CoA carboxylase. The activity of acetyl-CoA carboxylase is increased, but when the dietary deficiency of biotin produces biotin levels which are below 0-8 mug/g of liver, the activity of pyruvate carboxylase may be insufficient to completely metabolize pyruvate via gluconeogenesis. There is an increase in liver size and in the activities of enzymes involved in alternate pathways for the removal of pyruvate. Blood lactate accumulates and there is increased synthesis of fatty acids, and an accumulation of palmitoleic acid; these steps are accomplished by increased activities of at least the following enzymes: acetyl-CoA carboxylase, malate dehydrogenase (decarboxylating) (NADP+) and the desaturase enzyme. When the biotin level is below 0-35 mug/g of liver and the chick is subjected to a stress, physiological defence mechanisms of the chick may be inadequate to maintain homeostasis and they finally collapse, resulting in accumulation of triacylglycerol in the liver and blood; the chick is unable to maintain blood glucose levels and death occurs, often only a few hours after the imposition of the stress.
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PMID:Fatty liver and kidney syndrome in chicks. II. Biochemical role of biotin. 1 36

Liver slices from chicks affected by the fatty liver and kidney syndrome display an extremely low extent of hepatic gluconeogenesis which is associated with decreased activities of certain rate-limiting gluconeogenic enzymes. Pyruvate carboxylase activity is particularly severely affected, being less than 4% of control values. Incubation of affected slices in a biotin-containing nutrient medium restores both gluconeogenesis and pyruvate carboxylase actiivity (the latter to approx. 35% of the control valve). Activities of the other enzymes studied were not greatly affected by this treatment. Restoration of gluconeogenesis did not occur if biotin was excluded from the nutrient medium, nor was it prevented by protein-synthesis inhibitors. It is concluded that the syndrome involves the lack of available biotin in the liver rather than suppression of apocarboxylase synthesis.
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PMID:The biochemistry of fatty liver and kidney syndrome. Biotin-mediated restoration of hepatic gluconeogenesis in vitro and its relationship to pyruvate carboxylase activity. 18 41

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

1. Birds affected by fatty liver and kidney syndrome (FLKS) had elevated concentrations of serum Na+, K+, lactate, pyruvate and uric acid and reduced concentrations of serum HCO-3 and glucose. 2. Short-term treatment with biotin or animal tallow reduced the mortality from FLKS and prevented the clinical signs. 3. Lactic acidosis may be a major factor contributing to the mortality and physical symptoms observed in birds affected by FLKS. The lactic acidosis and the hypoglycaemia observed in FLKS are due primarily to an accumulation of pyruvate as a result of an insufficiency of biotin for normal pyruvate carboxylase activity.
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PMID:Clinical signs of fatty liver and kidney syndrome in broilers and their alleviation by the short-term use of biotin or animal tallow. 59 40

Varying degrees of biotin deficiency were induced by adding freeze-dried, raw egg white to the diet of broiler chicks. Aspects of liver metabolism were studied with reference to fatty liver and kidney syndrome. Mortality was low with 11.8 g egg white/kg diet, or less, but with 17.7 g/kg or more, mortality was very high. High mortality was observed with less than 0.33 microgram biotin/g liver. Associated with low concentrations of liver biotin were substantial increases in liver weight and lipid content in starved birds. The increased liver lipid content was not observed in birds fed ad libitum. The increased liver lipid content in biotin-deficient, starved birds was not reflected in the specific activities of hepatic lipogenic enzymes or hepatic lipogenesis in vivo measured by the incorporation of tritium from 3H-labelled water into liver lipid. Biotin deficiency affected the specific activities of the biotin-requiring enzymes, pyruvate carboxylase and acetyl CoA carboxylase, differently; the latter was unaffected whereas the former decreased concomitantly with liver biotin concentration.
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PMID:Biotin deficiency and liver metabolism in relation to fatty liver and kidney syndrome. 67 52

1. The changes in a number of metabolic measurements brought about by low-biotin diets associated with high and low incidences of fatty liver and kidney syndrome (FLKS) were studied in healthy 4-week-old broiler chicks. 2. Liver pyruvate carboxylase (pyruvate: CO2 ligase (ADP); EC 6.4.1.1) activity was low in birds fed on a diet causing a high incidence FLKS but the addition of fat or protein to this diet, to decrease the incidence of FLKS, increased enzyme activity. 3. Liver weights, blood lactate concentrations, plasma lactate dehydrogenase (L-lactate: NAD oxidoreductase; EC 1.1.1.27) activitvities and values for C16:1 : C18:0 fatty acid in liver, adipose tissue and plasma triglyceride were highest in birds fed on the high-FLKS diet and all measurements were negatively correlated with pyruvate carboxylase activity. 4. Birds with high plasma lactate dehydrogenase activity or triglyceride C16:1 : C18:0 values were the most likely to develop FLKS when fasted. 5. There was no evidence that increased liver weight was associated with increase activities of certain other liver enzymes. 6. It is concluded that FLKS occurs in birds with little or no hepatic gluconeogenic capacity via pyruvate carboxylase as a result of a dietary insufficiency of biotin but that the initiation of the syndrome in probably associated with the inhibition of other pathways of gluconeogenesis.
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PMID:Metabolic changes associated with the occurrence of fatty liver and kidney syndrome in chicks. 69 61

Biotin deficiency can be induced readily in monogastric animals and is accompanied by characteristic abnormalities. These include dermal lesions involving hyper- and parakeratosis and, in fur-bearing animals, alopecia and achromatricia. Biochemical changes include depressions in the activities of biotin-dependent enzymes and the metabolic pathways in which they are involved. However, it has been shown in chickens that the relative changes in the activities of these enzymes and the resultant manifestations of the deficiency can be markedly influenced by the dietary content of other nutrients such as protein or fat. Biochemical criteria are required for the diagnosis of subclinical deficiency and these are best-established for poultry. Blood pyruvate carboxylase activity is a good criterion in young birds. Biotin-responsive disorders have been identified in several species. The etiology of fatty liver and kidney syndrome in chickens is now largely understood and is an interesting example of how a combination of nutritional and environmental factors can result in sudden death in, until then, apparently healthy animals.
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PMID:Assessment of biotin deficiency in animals. 286 81

Fatty liver and kidney syndrome (FLKS), a naturally occurring but experimentally reproducible disease in chickens, has several clinical, pathological, and biochemical features in common with Reye's syndrome. Because of this, it has been suggested that FLKS may serve as an animal model of Reye's syndrome. We have examined, therefore, various parameters characteristic of Reye's syndrome in chickens affected with FLKS to further delineate the similarities and differences between the two disorders. Plasma glucose concentrations were significantly lower in chickens affected with FLKS which may be caused by the significantly reduced activity of pyruvate carboxylase in all FLKS-affected animals. The activity of propionyl CoA carboxylase was low in only the most severely affected chickens, and beta-methylcrotonyl CoA carboxylase showed no difference when compared with controls. This may be due to variable sensitivities of the three carboxylases to marginal biotin deficiency which occurs with FLKS. Plasma ammonia concentrations and activities of glutamic oxaloacetic transaminase and glutamic pyruvic transaminase, however, were not elevated in the affected birds. Histological changes in the liver and kidney were noted in affected chickens, but these changes were not identical with those observed in Reye's syndrome. Although the mechanisms of nitrogen elimination in fowl differ from those in humans, failure to demonstrate hyperammonemia, elevated serum transaminase activities, or similar histological changes in tissues of affected birds indicates that FLKS is not an appropriate model for the study of Reye's syndrome.
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PMID:Fatty liver and kidney syndrome in chickens as an animal model for Reye's syndrome. 664 49

A total of 560 day-old commercial broiler chicks were used in two experiments conducted to investigate the biotin requirement of broilers fed sunflower seed meal (SSM) based diets. Two basal biotin-deficient diets based on dehulled (Experiment 1) and non-dehulled (Experiment 2) SSM were each supplemented with graded levels of biotin so that the rations had 40, 80, 120, 160, 200, 240 and 280 mcg/kg feed. Therefore a total of 14 treatments were tested. Each treatment was given to duplicate floor pens with 20 chicks each for a period of 28 days. Estimation of the live weights, live weight gain, feed intake, blood glucose and free fatty acid concentrations, lipid contents and weights of liver and kidney, and liver pyruvate carboxylase activity and the records of incidence of dermal lesions, fatty liver and kidney syndrome (FLKS) mortality and leg deformities indicated that in the case of dehulled SSM, dietary biotin of of 160 mcg/kg feed was marginal while at least 200 mcg/kg appeared to be needed for optimum performance of the birds. When non-dehulled SSM was incorporated in the diet, 200 mcg biotin/kg feed was found to be the lowest dietary level needed. However, as it seems that better results could be obtained with higher levels, 240 mcg biotin/kg with non-dehulled SSM is being recommended.
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PMID:Studies on the biotin requirement of broilers fed sunflower seed meal based diets. 748 81

The effects of glucagon infusions on expression of mRNA for enzymes that regulate gluconeogenesis were studied in lactating cows. Normal cows and cows with fatty liver that were susceptible to ketosis were assigned to either glucagon-treated or control groups. Glucagon at 0 or 10 mg/d was infused for 14 d beginning at d 21 postpartum. In normal cows, glucagon infusions increased concentrations of both plasma glucagon and glucose, which caused plasma insulin to increase. Consequently, hepatic phosphoenolpyruvate carboxykinase mRNA decreased during wk 1 of glucagon infusions. Glucagon infusions into cows with fatty liver also increased plasma glucagon and glucose, but concentrations of plasma insulin and hepatic phosphoenolpyruvate carboxykinase mRNA did not change. More phosphoenolpyruvate carboxykinase mRNA was present in the livers of cows with fatty liver than in livers of normal cows. In a follow-up experiment with midlactation cows, 3.5-h infusions of glucagon at 14 mg/d increased plasma glucose and insulin and decreased plasma nonesterified fatty acids and hepatic glycogen. Hepatic phosphoenolpyruvate carboxykinase mRNA was decreased 41%, pyruvate carboxylase mRNA was increased 50%, but fructose-1,6-bisphosphatase mRNA did not change. We conclude that the expression of the hepatic phosphoenolpyruvate carboxykinase gene in normal cows is inhibited by insulin to balance elevated carbohydrate status during glucagon infusions; however, inhibited expression of hepatic phosphoenolpyruvate carboxykinase mRNA probably is not involved in the pathogenesis of lactation ketosis.
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PMID:Regulation of messenger ribonucleic acid expression for gluconeogenic enzymes during glucagon infusions into lactating cows. 1038 1


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