Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three cases of severe anorexia are reported. It results in a strong protein malabsorption with hepatic steatosis and in a syndrome of mental depression which needed the re-establishment of the intestinal-continuity. Although a mild post-operative anorexia is regular and contributes to the weight loss, massive anorexia must be considered as a new and redoubtable unpredictible complication of the surgical treatment for obesity, which may hinder the intestinal adaptation and increase the protein malabsorption.
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PMID:[Anorexia: a redoubtable complication of the surgical treatment for obesity after jejuno ileal by-pass (author's transl)]. 9 23

Experiments were conducted from 1968 to 1974 to investigate reproductive complications and mortality in mink fed Great Lakes coho salmon and to ascertain the effects of polychlorinated biphenyls (PCB's) on this fur bearer. The results of mink feeding trials indicated that coho salmon, as such, were not responsible for the loss of reproduction in the adult, or the kit mortality. Mink diets that contained other species of Great Lakes fish caused similar reproductive complications, but to a lesser degree. Rancidity, mercury poisoning and chlorinated hydrocarbon pesticide contamination of the fish were all discounted as being responsible for the problem. The clinical signs and lesions noted in mink that died while receiving diets that contained Lake Michigan coho salmon were very similar to those observed in mink fed on rations that contained supplemental PCB's. These included anorexia, blood stools, fatty liver, kidney degeneration, and hemorrhagic gastric ulcers. Analyses of tissues from mink that died when fed 30% Lake Michigan coho salmon or 30 ppm supplemental PCB diets showed similar PCB residues. PCB toxicity experiments revealed that mink are very sensitive to these compounds and that the lethal dose varied inversely with the chlorine content of the PCB's although only Aroclor 1254 exerted a detrimental effect on reproduction when fed at a low level (2 ppm) for 8 months. The reproductive failure encountered in feeding mink Lake Michigan coho salmon and Aroclor 1254 was shown to be of a non-permanent nature.
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PMID:Current status of PCB toxicity to mink, and effect on their reproduction. 40 55

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

Woodchucks were used to study the antiviral activity and toxicity of fialuridine (FIAU; 1,-2'deoxy-2'fluoro-1-beta-D-arabinofuranosyl-5-iodo-uracil). In an initial experiment, groups of six chronic woodchuck hepatitis virus (WHV) carrier woodchucks received daily doses of FIAU by intraperitoneal injection for 4 weeks. At 0.3 mg/kg/d, the antiviral effect was equivocal, but at 1.5 mg/kg/d, FIAU had significant antiviral activity. No evidence of drug toxicity was observed during the 4-week period of treatment or during posttreatment follow-up. In a second experiment, groups of nine WHV carriers or uninfected woodchucks were given 1.5 mg/kg/d of FIAU orally for 12 weeks, and the results compared with placebo-treated controls. After 4 weeks, the serum WHV-DNA concentration in the FIAU-treated carrier group was two to three logs lower than that in the placebo-treated group. After 12 weeks of FIAU treatment, serum WHV DNA was not detectable by conventional dot-blot analysis, hepatic WHV-DNA replicative intermediates (RI) had decreased 100-fold, and hepatic expression of WHV core antigen was remarkably decreased. No evidence of toxicity was observed after 4 weeks, but, after 6 to 7 weeks, food intake decreased and, after 8 weeks, the mean body weights of woodchucks treated with FIAU were significantly lower than controls. Anorexia, weight loss, muscle wasting, and lethargy became progressively severe, and all FIAU-treated woodchucks died or were euthanized 78 to 111 days after treatment began. Hepatic insufficiency (hyperbilirubinemia, decreased serum fibrinogen, elevated prothrombin time), lactic acidosis, and hepatic steatosis were characteristic findings in the final stages of FIAU toxicity in woodchucks. The syndrome of delayed toxicity in woodchucks was similar to that observed previously in humans treated with FIAU, suggesting that the woodchuck should be valuable in future investigations of the molecular mechanisms of FIAU toxicity in vivo and for preclinical toxicological evaluation of other nucleoside analogs before use in patients.
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PMID:Antiviral activity and toxicity of fialuridine in the woodchuck model of hepatitis B virus infection. 965 11

A 3-year-old female llama that was 3 months into her first lactation and 10 weeks pregnant was evaluated for anorexia of 24 hours' duration. On physical examination, the llama was in lateral recumbency, bradycardic, tachypneic, and hyperthermic. Palpation per rectum confirmed the presence of a possible dry fecal mass in the spiral colon. A tissue biopsy specimen of the liver was obtained, and histologic examination revealed moderate diffuse lipid accumulation within the hepatocytes. Lactated Ringer's solution was administered for rehydration, and partial parenteral nutrition was then initiated. Hepatic lipidosis is a disease characterized by abnormal accumulation of lipid in the liver and is associated with high mortality in camelids. Anorexia associated with hepatic lipidosis promotes further lipid mobilization and fatty infiltration of the liver. Partial parenteral nutrition with enteral supplementation may be used to maintain adequate energy intake and minimize further lipid mobilization. The distinctive metabolism of camelids may require higher amino acid supplementation relative to nonprotein calories in parenteral solutions than those traditionally provided to other species. Treatment with insulin may be effective
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PMID:Nutritional support for treatment of hepatic lipidosis in a llama. 1112 46

Acute liver disease was diagnosed in three pregnant patients: two 30-year-old women had a 'haemolysis, elevated liver enzymes, low platelets' (HELLP) syndrome and acute fatty liver of pregnancy, respectively, and a 20-year-old woman had acute liver failure due to acute hepatitis B. The first two patients had a caesarean section, the third one delivered her child, which died spontaneously shortly after birth at a gestational age of 23 weeks. She was then treated by liver transplantation. All three patients left the hospital in good condition. Liver diseases in pregnancy may be pregnancy-related, e.g. the HELLP syndrome and acute fatty liver of pregnancy, but they may also be coincidental phenomena, e.g. viral hepatitis. The HELLP syndrome is often associated with pre-eclampsia, and presents with epigastric pain and thrombocytopenia with haemolysis. Acute fatty liver disease and acute liver failure due to hepatitis present with liver insufficiency characterised by anorexia, nausea, coagulopathy, hypoglycaemia and elevated serum ammonia levels. Management depends on the diagnosis and the gestational age; pregnancy complicated by acute fatty liver disease should be terminated while pregnancy complicated by the HELLP syndrome early in pregnancy may be maintained to improve the outcome of the foetus. In acute liver failure due to viral hepatitis, termination of pregnancy alone does not affect the disease.
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PMID:[The pregnant patient with acute liver disease]. 1253 8

Hepatic lipidosis, a hallmark lesion of lipid mobilization disorders in ruminants, was noted in four 3-year-old, pregnant bison (Bison bison) after periods of anorexia that progressed to recumbency and death. The affected bison were part of a herd at the National Animal Disease Center (NADC) that was used for brucellosis vaccine research. Microscopically, the liver contained swollen hepatocytes with numerous, variably sized, round, smoothly contoured vacuoles that displaced cytoplasmic structures. Hepatocytes in all zones of the lobule were affected equally. Hypoglycemia, decreased total carbon dioxide, elevated gamma-glutamyltransferase, elevated alkaline phosphatase, and increased nonesterified fatty acid levels were noted. As in the case of cattle, altered nutritional demands of late gestation combined with management factors such as obesity, nutrition, stress, and concomitant disease may be critical in the pathophysiology of lipid mobilization disorders in bison. Additionally, stressors unique to this research herd likely contributed to fatal hepatic lipidosis.
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PMID:Hepatic lipidosis in pregnant captive American bison (Bison bison). 1242 37

Obesity and its attendant disorders, such as type 2 diabetes, are global health problems. We previously reported that C75, an inhibitor of fatty acid synthase (FAS) and stimulator of carnitine palmitoyltransferase I (CPT I), caused anorexia and profound weight loss in lean and genetically obese mice. To approximate human obesity, we utilized a chronic C75 treatment model for diet-induced obese (DIO) mice. Chronic C75 treatment decreased food consumption and increased energy expenditure due to increased fatty acid oxidation in both DIO and lean mice. There was a substantial loss of adipose tissue and resolution of hepatic steatosis in C75-treated DIO mice. Analysis of changes in the expression of hypothalamic neuropeptides demonstrated that the reduced food consumption in C75-treated DIO mice was accompanied by an increase in cocaine and amphetamine-related transcript expression but not by changes in neuropeptide Y such as seen with acute C75 treatment of lean mice. Inhibition of FAS and stimulation of CPT I provide a means to achieve stable, sustained weight loss in DIO mice.
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PMID:Chronic C75 treatment of diet-induced obese mice increases fat oxidation and reduces food intake to reduce adipose mass. 1473 2

Anorexia in obese cats may result in feline hepatic lipidosis (FHL). This study was designed to determine plasma lipids and lipoprotein profiles in queens at different stages during experimental induction of FHL (lean, obese, FHL), and after 10 weeks of treatment. Results were compared with those obtained from lean queens of same age fed the same diet but at a maintenance level, once a day. Hepatic lipidosis led to an increase in plasma triacylglycerol (TG), very low density lipoprotein (VLDL) and low density lipoprotein (LDL), and an enrichment of LDL with TG and of high density lipoprotein (HDL) with cholesterol, suggesting that VLDL secretion is enhanced, VLDL and LDL catabolism is lowered, and lipoprotein exchanges are impaired in FHL. This study also showed that cholesterolaemia is increased in cats fed at a dietary rhythm of one meal per day compared to ad libitum feeding.
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PMID:Plasma lipids, lipoprotein composition and profile during induction and treatment of hepatic lipidosis in cats and the metabolic effect of one daily meal in healthy cats. 1505 30

A 3-year-old intact female domestic shorthair cat was presented for the evaluation of a palpable intra-abdominal mass in the left caudal abdomen. The cat had a history of anorexia, depression and prolonged estrus over a period of about 1 month. Smears prepared from a fine needle aspirate of the mass revealed large round to oval cells arranged individually or in loose clusters surrounded by pink, fibrillar matrix material. Cytoplasm was basophilic, with many variably-sized vacuoles and variable numbers of small purple granules. The vacuoles within the cells were strongly positive with Oil-Red-O stain. The cytologic features were most suggestive of a neoplasm of epithelial cell origin or inadvertent aspiration of a fatty liver. At laparotomy, the mass was found to involve the left ovary. Histologically, the tumor consisted of dense sheets and nests of irregular polyhedral, pleomorphic cells with abundant, finely vesiculated cytoplasm. The tumor cells were separated into lobules by strands of connective tissue. Based on histologic evaluation, a diagnosis of ovarian luteoma was made. In this report, we document the cytologic and histologic features of an uncommon feline tumor, a luteoma, and address its possible misdiagnosis as hepatic lipidosis when using cytology alone to make a diagnosis.
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PMID:Intra-abdominal mass aspirate from a cat in heat. 1613 78


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