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

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

Commercial laying hens with Fatty Liver Syndrome had greatly elevated levels of serum calcium and cholesterol. Most of the hens with the elevated serum calcium and cholesterol were out of production, but some were still in production. Hens with elevated calcium and cholesterol levels had extremely large combs and excessive deposits of fat in the abdomen.
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PMID:Serum and body characteristics of laying hens with fatty liver syndrome. 53 88

The effect of feeding biotin and palm kernel oil to broiler chicks on the appearance of Fatty Liver and Kidney Syndrome (FLKS) was investigated. A total of 480 broiler chicks was divided into two equal batches each of which was divided into 6 groups of 40 chicks per group. Each group was further subdivided into equal units of 20 chicks. Six dietary levels of biotin (40, 80, 120, 160, 200, and 240 mcg/kg feed) were given to the first batch of chicks, while the second batch had 2% palm kernel oil added to the six dietarybiotin levels. These two basic rations were supplemented with biotin in order to obtain six levels of the vitamin in the rations. The results showed that the 2% palm kernel oil forage affected FLKS mortality and the minimum biotin requirement. FLKS mortality was significantly reduced in case of palm kernel oil supplement. A lower amount of biotin (120 mcg/kg feed) was needed in case of palm kernel oil supplement-as compared with the necessary biotin (160 mcg/kg feed)-in order to prevent FLKS mortality when palm kernel oil was not contained in the rations. The biochemical analysis of the liver and kidney syndrome-coupled with the correlation and regression analysis of the data collected-showed that a minimum of 120 mcg/kg feed was needed by broiler chicks for the prevention of FLKS.
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PMID:Effect of dietary palm kernel oil and biotin on the fatty liver and kidney syndrome in broiler chicken. 261 3

Drug injury of the liver presents as I. functional disorder without jaundice; 2. predominant cholostatic disease; 3. predominant hepatitic disease; 4. a combination of 2 und 3.--A predictable dose related direct toxic injury can be differentiated from an unpredictable dose independent indirect injury mostly of the hypersensitivity type. Special varieties are severe fatty liver, peliosis, Budd-Chiari-Syndrome, liver tumors and granulomas. The diagnosis can be proven by reexposition or better--by the in vitro lymphocyte stimulation test. --There is no specific treatment apart from stopping the responsible drug. Prognosis is good but in some cases a chronic course develops presenting as chronic aggressive hepatitis or cirrhosis.
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PMID:[Liver damage caused by drugs]. 716 50

Lipid metabolism in the cells of the renal proximal convoluted tubules (PCT) was investigated in healthy fowls and in fowls with the Fatty Liver and Kidney Syndrome (FLKS). The tissue was fixed at 10-25 min intervals after intravenous injection of 3H-oleic acid. The distribution of autoradiographic grains was analysed by the "circle method". In normal cells most of the silver grains were associated with the cytoplasmic organelles. Lipid droplets and Golgi elements had the highest specific activity relative to the nuclear activity, which was little above background level. Lysosome-like bodies and mitochondria had lower values. In the cells of the FLKS-affected birds a large porportion of the grains was located over the lipid droplets, which are abundant in this condition. The specific activity of the cytoplasmic organelles was barely 2-fold higher than the nuclear activity. The results suggest that there is a diminished incorporation of esterified fatty acids by the organelles of these cells and that the excess is transferred to the lipid droplets. The identity of low electron density particles observed in the PCT cell of severely affected birds is discussed.
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PMID:Incorporation of 3H-oleic acid by the proximal convoluted tubule cells of the chick (Gallus domesticus). Electron microscopic autoradiographic study. 740 48

Preeclampsia is a multisystem disorder of pregnancy whose clinical presentation is related to the importance and the extent of maternal microvasculature damage. 16 patients with preeclampsia, thrombocytopenia (< 100,000/mm3), elevated liver enzymes and hemolysis are described. Weinstein in 1982 assigned the acronym of Hellp syndrome for this clinical presentation of preeclampsia. This syndrome was seldom recognized during the first years of the study but was diagnosed later on, in 1 pregnancy out of 600 parturitions and in 5% of preeclampsia in 1991. Two out of the patients developed eclamptic seizures. The mode of delivery was as follows: 9 out of 16 had an emergency Caesarean section; the 7 other patients had vaginal delivery after induction of labor. Delivery occurred before 32 weeks of gestation for 6 out of 17 newborns. Outcome was good for 14 of the 17 newborns (one twin pregnancy). Two fetuses died: one in utero and one during interruption of the pregnancy at 24 weeks of gestation. A small for gestational age preterm of 32 weeks died on his second day of life. Early diagnosis of Hellp Syndrome, especially when abdominal pains are present, allows a prompt management of these patients, including delivery, which appeared in our experience, the only way to avoid fetomaternal complications. The thrombotic microangiopathics and acute fatty liver of pregnancy are potential imitations of Hellp syndrome and they must be considered for differential diagnosis. The frequency of Hellp Syndrome varies from one study to another. It can be increased up to 6 fold if referred to the number of pregnancies and up to 3 fold if referred to the number of preeclampsias. These differences can be real but may be due to bias related to differences in practice between centers and also differences in definitions of Hellp Syndrome and preeclampsia.
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PMID:[The Hellp syndrome: a frequent (?) obstetric emergency]. 835 77

We report on a 33-year-old male patient with generalized acquired lipodystrophy, insulin resistant diabetes mellitus and acanthosis nigricans (Lawrence Syndrome). First probable symptoms of lipodystrophy (weight loss, shrinkage of subcutaneous fatty tissue, and loss of muscular strength) became evident three years ago, with the onset of diabetes mellitus occurring about six months later. The patient suffered from the following clinical symptoms: IDDM with increasing insulin-requirement, extreme reduction of fatty tissue, fatty liver hepatitis with elevated liver enzymes, glomerulopathy, muscular and neuropathic pains, as well as hypertriglyceridaemia. A basal C-peptide concentration is rather high. Definitely, the endogenous insulin secretion is increased. In other words, insulin resistance is documented. In an effort to identify the pathogenetic mechanisms of lipoatrophic diabetes mellitus in this patient and to develop a therapeutic strategy, antibodies against different tissues and endocrinologic regulation were investigated. It was possible to demonstrate the presence of serum autoantibodies against lipocytes of the subcutis and other tissues, against hepatic stellate cells, together with autoantibodies against different endocrine organs. By studying the basis of diabetic abnormalities relating to the growth hormone (GH), the insulin-like growth factor (IGF) dynamics in this patient, i.e. reductions of GH, IGF-I, IGF-II, IGF-Binding protein (IGF-BP) 2 and IGF-BP 3, were detected. An immunosuppressive treatment strategy was not beneficial.
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PMID:Dysregulation of insulin-like growth factors in a case of generalized acquired lipoatrophic diabetes mellitus (Lawrence Syndrome) connected with autoantibodies against adipocyte membranes. 951 65

Acute fatty liver of pregnancy is a rare disease which may be letal if diagnosis is missed. The pathogenesis is not completely clear, but there is some evidence that some cases have been associated with a genetic deficiency of fatty acid beta-oxidation. Other predisposing factors include primiparity, multiple pregnancy, male fetal sex and pre-eclampsia. Clinical presentation and laboratory findings are often unspecific. Increasing serum aminotransferases are characteristic in the early stage of the disease. Liver biopsy establishes the diagnosis and typically shows microvesicular, centrilobular fatty changes of hepatocytes. Differential diagnosis includes the HELLP-Syndrome, cholestasis of pregnancy, pre-eclampsia and viral or drug induced hepatitis. Without adequate treatment liver failure with coagulopathy and encephalopathy may develop. Two cases of acute fatty liver in pregnancy in an early stage are presented. Clinical and histopathological findings as well as diagnostic and therapeutic procedures are discussed.
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PMID:[Acute fatty liver in pregnancy: clinical and histopathological course. Case report]. 1188 62

1. The rate of thrombin generation in plasma from Fatty Liver Haemorrhagic Syndrome-susceptible laying hens (FLHS, UCD-003) is more rapid than in plasma from age-matched normal Single Comb White Leghorn (SCWL) laying hens. 2. The rate of thrombin generation in plasma was determined by measuring the biological activity of the specific coagulation proteins, Factors V, VII, VIII, IX and X. 3. The higher activity of Factors V, VII and X in FLHS-susceptible laying hens compared with normal SCWL hens remained consistent after plasma lipid concentrations were reduced. 4. Analysis of the fatty acid composition of plasma phospholipids showed that in normal SCWL laying hens phosphatidylethanolamine contained C18:3n3 whereas it contained C20:3n3 in FLHS-susceptible laying hens. 5. The results suggest that alterations in the composition of the phospholipids that are essential cofactors in the biochemical reactions involved in thrombin generation may be a contributing factor in the development of FLHS.
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PMID:Comparison of the coagulation profile of fatty liver haemorrhagic syndrome-susceptible laying hens and normal laying hens. 1458 54

The incidence of obesity has increased dramatically in recent years, making it one of the most pressing public health concerns worldwide. Obesity is commonly associated with comorbid conditions, most notably diabetes, coronary artery disease, and hypertension, and the coexistence of these diseases has been termed the Metabolic Syndrome. The identification of the hormone leptin provided a molecular link to obesity. Leptin is recognized as the central mediator in an endocrine circuit regulating energy homeostasis. Leptin administration leads to hypophagia, increased energy expenditure, and weight loss, while leptin deficiency enacts an adaptive response to starvation manifested by hyperphagia, decreased energy expenditure, and suppression of the neuroendocrine axis. While elucidation of leptin's role has permitted a more detailed view of the biology underlying energy homeostasis, most obese individuals are leptin resistant. A more complete understanding of the molecular components of the leptin pathway is necessary to develop effective treatment for obesity and the Metabolic Syndrome. The identification and role of one such component, stearoyl-CoA desaturase-1 (SCD-1), is reviewed here. Leptin's actions are not due to its anorectic effects alone. Leptin also mediates specific metabolic effects, including the potent depletion of triglyceride from liver and other peripheral tissues. To explore the molecular basis by which leptin depletes hepatic lipid, we used oligonucleotide arrays to identify genes in liver whose expression was modulated by leptin treatment. An algorithm was created that identified and ranked genes specifically repressed by leptin. The gene ranking at the top of this list was SCD-1, the rate limiting enzyme in the biosynthesis of monounsaturated fats. SCD-1 was specifically repressed during leptin-mediated weight loss, and mice lacking SCD-1 showed markedly reduced adiposity on both a lean and ob/ob background (ab(J)/ab(J); ob/ob), despite higher food intake. ab(J)/ab(J); ob/ob mice also showed a complete correction of the hypometabolic phenotype and hepatic steatosis of ob/ob mice, suggesting that fatty acid oxidation is enhanced in the absence of SCD-1. These findings indicate that pharmacologic manipulation of SCD-1 may be of benefit in the treatment of obesity, diabetes, hepatic steatosis, and other components of the Metabolic Syndrome.
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PMID:Stearoyl-CoA desaturase-1 and the metabolic syndrome. 1468 58


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