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

Splanchnic metabolism was studied to quantify changes underlying the fatty liver, hyperlipemia, and hypoglycemia produced by ethanol. Four subjects fasted for 15 h were compared with five subjects fasted for 69 h under basal conditions and during continuous intravenous infusion of sufficient ethanol to give a concentration of 3-5 mM in arterial blood plasma. Splanchnic storage of fatty acids was estimated from the difference between uptake of FFA and secretion of derived products. Basal values for splanchnic uptake of FFA were twofold higher after the 69-h fast while splanchnic storage of fatty acids and production of ketone bodies increased threefold. Values for basal secreation into the blood of triglycerides derived from FFA were similar in the two groups. In both nutritional states, the fraction of FFA taken up in the splanchnic region oxidized to ketone bodies and to CO2 fell when ethanol was given because of preferential oxidation of ethanol to acetate, and the fraction esterified rose. However, systemic transport and splanchnic uptake of FFA fell with ethanol in subjects fasted 15 h, so that neither storage of triglycerides in splanchnic tissues nor secretion into the blood increased. In subjects fasted 69 h, ethanol increased transport of FFA and splanchnic storage of fat. In all but one subject it also increased secretion of triglycerides into the blood. The concentration of glucose in blood fell during ethanol infusion in all five subjects undergoing the 69-h fast. Mean splanchnic glucose production was maintained at about one-half of the pre-ethanol value, despite virtual cessation of splanchnic uptake of lactate and of those amino acids that are metabolized via malate. Quantitative estimates of extrasplanchnic metabolism suggest that enhanced formation of alpha-glycerophosphate from glucose, in addition to impaired hepatic gluconeogenesis, may contribute to ethanol-induced hypoglycemia in man.
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PMID:Effects of a 3-day fast and of ethanol on splanchnic metabolism of FFA, amino acids, and carbohydrates in healthy young men. 17 79

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

Plasma glucose, free fatty acid and triglyceride levels were measured during the onset of fatty liver and kidney syndrome in chicks. Intial studies indicated that behavioural and clinical changes characteristically associated with the syndrome were observed only during the 24 h preceding death. A more detailed examination of the blood changes was made on fasted birds. Typically, affected birds could be distinguished from healthy fasted birds by a hypoglycaemia which developed within 2.5 h of the removal of food, and a slightly higher and more sustained elevation of free fatty acid levels. Triglyceride values were not generally different from those found in normal birds. Although moderate to large amounts of lipid were occasionally observed in the kidneys of healthy fasted birds, only in affected birds was significant lipid infiltration of the kidneys associated with a similar level of lipid infiltration of the liver. In extreme cases death from fatty liver and kidney syndrome could occur within 4 h of the removal of food.
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PMID:Changes in plasma lipid and glucose levels during the onset of fatty liver and kidney syndrome in chics. 60 94

A case of a 26-year-old woman who presented at 38 weeks of gestation with severe hepatitis B complicated by disseminated intravascular coagulation (DIC) and hypoglycemia is reported. The clinical features of the illness suggested acute fatty liver of pregnancy. Cesarean section was followed by resolution of the coagulopathy and the hypoglycemia. Both mother and infant survived and remain well. The diagnosis of hepatitis B was confirmed by a transiently positive hepatitis B surface antigen and percutaneous liver biopsy. This case emphasizes the difficulty in distinguishing acute viral hepatitis from acute fatty liver of pregnancy. In addition, the predominant features of DIC and hypoglycemia in our case are reported.
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PMID:Viral hepatitis in pregnancy with disseminated intravascular coagulation and hypoglycemia. 63 35

Studies of the general histopathology of the fatty liver and kidney syndrome in chickens have shown abnormal accumulations of the lipid in a variety of organs but no degenerative or inflammatory reactions. Lipid was found in some skeletal muscles, alimentary tract, autonomic ganglia, central nervous system and pineal gland as well as in the liver, kidney and heart. Small amounts of lipid were sometimes seen in the exocrine pancreas, adrenal medulla and epithelium of the thyroid follicles. Lipid deposits in the liver were primarily associated with the hepatic structural unit. The glycogen content of the hepatic cell was reduced. The lipid-metabolising gastrocnemius muscle contained abnormal amounts of lipid but this did not apply to the carbohydrate-metabolising pectoralis major muscle. The thymus did not contain excessive lipid but was significantly smaller in affected than in control birds of similar ages. There was loss of tinctorial distinction between the cortex and medulla of the adrenal gland associated with decreased basophilia of the latter region. Many of these morphological changes can be correlated with previously reported biochemical findings and they are discussed in relation to the hyperlipaemia and hypoglycaemia which characterise the disease.
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PMID:The histopathology of fatty liver and kidney syndrome in chicks. 116 22

A case of sudden death associated with fatty liver and encephalopathy is described in a 4-year old white boy with medium-chain acyl-coenzyme A dehydrogenase (MCAD) deficiency. The death was caused by hypoglycemia triggered by fasting and vomiting associated with a minor viral infection. The differential diagnosis of the hepatoencephalopathy is discussed in relation to other conditions, especially Reye's syndrome. The forensic pathologist should be familiar with MCAD and other deficiencies of beta-oxidation of fatty acids as a cause of sudden unexpected death in children in order to advise parents in genetic counseling to prevent disability or death of other affected, but still asymptomatic siblings.
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PMID:Fatty liver, encephalopathy, and sudden unexpected death in early childhood due to medium-chain acyl-coenzyme A dehydrogenase deficiency. 128 65

We report the case of a mother who developed fulminant hepatic failure with hypoglycaemia, coagulopathy, Grade III hepatic encephalopathy, two days after the delivery of her fourth child. She had complained of pruritus for the final two weeks of pregnancy. She received supportive medical management within a critical care unit, and the hepatic failure resolved completely within 48 hours. Liver biopsy confirmed the diagnosis of acute fatty liver of pregnancy. This case is unusual in that this patient deteriorated markedly following delivery, at a time when spontaneous recovery is normally expected.
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PMID:Fulminant hepatic failure in a young mother. 153 May 36

A case of clinically diagnosed acute fatty liver of pregnancy (AFLP) is reported. Hypoglycemia and coagulopathy were predominant in the clinical course. Serial studies on blood chemistry, especially blood glucose and coagulation parameters, in association with virus serology and ultrasound, can rule out common causes of jaundice in pregnancy. This contributes to reliability of the clinical diagnosis of AFLP in the absence of liver biopsy, and ensures adequate management of the patient.
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PMID:[Acute fatty liver of pregnancy--differential diagnosis and supportive therapy]. 160 87

In Japan, acute encephalopathy with hepatic steatosis resembling Reye's syndrome has been reported to occur after treatment with the pantothenic acid antagonist, calcium hopantenate. We studied the causal relationship and the pathogenesis in dogs. The agent was administered to seven dogs at increasing doses over a period of 8 weeks. Anorexia, vomiting, and diarrhea were common clinical findings. In four dogs, coma suddenly developed after the appearance of gastrointestinal signs. Three animals died during periods when they were not under direct observation. The effects of the agent appear to be related to dose. Laboratory findings representing significant changes at the time of coma included hypoglycemia, leukocytosis, hyperammonemia, hyperlactatemia, and elevated levels of serum transaminases. Microvesicular hepatic steatosis and mitochondrial abnormalities were consistent pathological findings. The hepatic mitochondria were enlarged and characterized by an increased number of cristae and the presence of crystalloid inclusions. In a second group of four dogs, pantothenic acid was given in addition to and in the same amount as calcium hopantenate at increasing doses over a period of 8 weeks. All four dogs survived the 8 weeks and only one developed mild anorexia. No significant biochemical changes were found and neither hepatic steatosis nor mitochondrial abnormalities were observed. The addition of pantothenic acid prevented the development of the disorder in the four animals. These results show that calcium hopantenate produces acute encephalopathy with hepatic steatosis in dogs, by inducing a deficiency of pantothenic acid. The hepatic mitochondrial changes of this reaction differ from those of Reye's syndrome.
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PMID:Acute encephalopathy with hepatic steatosis induced by pantothenic acid antagonist, calcium hopantenate, in dogs. 188 58


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