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)

Rapeseed meal hepatosis was produced by feeding high and low glucosinolate meals as a source of protein (about 200 g kg-1 diet) but could not be distinguished histologically from fatty liver-haemorrhagic syndrome which occurred in birds on the control diet. Both types of meal increased haemorrhage, reticulolysis and lymphoproliferation in the liver, reduced the packed cell volume and caused thyroid enlargement. Haemorrhages emanated from ruptured intrahepatic portal veins, capillaries and sinusoids and were associated with degenerative changes in vessel walls. Haemorrhage and reticulin scores were correlated. Parenchymal necrosis occurred only around large haematomas and caused increased aspartate transaminase activity in the plasma. Both meals also caused hyperglycaemia and reduced the plasma triglyceride content. Only the high glucosinolate meal decreased egg production, caused liver enlargement and reduced the plasma urate level. The addition of myrosinase enhanced its effects on egg production and packed cell volume but did not increase its hepatotoxicity.
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PMID:Rapeseed induced liver haemorrhage, reticulolysis and biochemical changes in laying hens: the effects of feeding high and low glucosinolate meals. 646 74

Serum concentrations of conjugated cholic acid determined radioimmunologically were investigated for 3 hours after a test meal in 62 patients with fatty liver, 70 patients with chronic hepatitis and 30 patients with liver cirrhosis. Values were compared with results of further data from chemical pathology. Increased fasting bile acid values were found in 18% of patients with fatty liver, 13% with chronic hepatitis and in 70% with cirrhosis. Following the test meal maximum concentration increase of cholic acid conjugates was obtained after one hour. 70.5% of patients with fatty liver, 80% of patients with chronic hepatitis and 97% of patients with cirrhosis were identifiable by increased bile acid levels. Postprandial serum bile acid levels therefore have a higher sensitivity for diagnosis of liver disease than bilirubin, glutamic-oxaloacetic transaminase, alkaline phosphatase or gamma-glutamyl transferase.
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PMID:[Value of serum levels of conjugated cholic acid in the diagnosis of liver disease (author's transl)]. 710 4

A high energy maize diet produced a higher incidence of fatty liver-haemorrhagic syndrome than a low energy barley diet when the diets were fed during the summer. The triglyceride content of the liver increased with the liver haemorrhage score and in hens with the highest scores there was evidence of hepatic hyperplasia. They also had high activities of aspartate transaminase and cholinesterase in the plasma and a low activity of sorbitol dehydrogenase. There was no increase in plasma endotoxin levels as the syndrome developed or any significant variation in these levels with the haemorrhage score, the triglyceride content of the liver or plasma enzyme activities. It was concluded that the steatosis does not impair the ability of the liver to inactivate endotoxins of enteric bacteria and that these toxins are not involved in the pathogenesis of the syndrome.
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PMID:Bacterial endotoxins and the pathogenesis of fatty liver--haemorrhagic syndrome in the laying hen. 732 74

Morbid obesity has been associated with hepatic steatosis and occasional cirrhosis. Despite producing weight loss, intestinal bypass procedures formerly performed to correct morbid obesity, often worsened steatosis and fibrosis, and occasionally resulted in hepatic failure. Current surgical procedures of choice for morbid obesity involve gastric bypass with gastrojejunostomy. Ninety-one liver biopsies taken at the time of gastric bypass for morbid obesity (mean body weight 125.8 kg), and 106 biopsies taken from the same patients from 2 to 61 months later (mean body weight 89.4 kg) were studied. Steatosis and perisinusoidal fibrosis were assessed in histologic sections. Serum albumin, alkaline phosphatase, aspartate aminotransferase (AST), and total bilirubin levels were measured before most biopsies were taken. Both pre- and post-gastric bypass hepatic steatosis varied directly with body weight (r = .5231, P < .001). Steatosis varied inversely with length of time after gastric bypass (r = .4590, P < .001). Of the original biopsies, 37% had lipid vacuoles in at least 26% of hepatocytes. After gastric bypass, 65 patients had reduced steatosis, 18 patients with no steatosis, and 5 patients with minimal steatosis had no change, and 3 patients had increased steatosis. Pre-gastric bypass biopsies from 13 patients had perisinusoidal fibrosis (PSF) that was marked with bridging in three patients, was moderate in one patient, and slight in nine patients. Following gastric bypass, PSF was eliminated in 10 patients, reduced in one patient, and the same in two patients. One patient developed PSF after gastric bypass. Of the three patients who had undergone previous intestinal bypass procedures, two had slight PSF in the biopsies taken at the time of gastric bypass, and one of these had slight PSF in the follow-up biopsy. Serum biochemical abnormalities tended to be slight. Before gastric bypass, serum albumin was low in 11% of cases, alkaline phosphatase was high in 14% of cases, AST was high in 11% of cases, and total bilirubin was high in 1% of cases. After gastric bypass, there was a small reduction in mean serum albumin from 43 g/L before to 41 g/L afterward (P < .05), and a slight rise in mean total bilirubin from 7.0 mumol/L before to 9.6 mu mol/L afterward (P < .01). Most hepatic fatty change and probably some PSF occurring in morbidly obese persons is reduced or eliminated with weight loss following gastric bypass surgery.
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PMID:Regression of hepatic steatosis in morbidly obese persons after gastric bypass. 761 Nov 76

Ultrasonic and laboratory studies were performed in 816 white-collar workers over 35 years old who received health examination. Prevalence of fatty liver diagnosed by ultrasonography was 17.9% in all subjects and was maximum (24.4%) in males 45-49 years of age. Obesity index and body mass index were higher in fatty liver than in normal controls. Serum levels of glutamate pyruvate transaminase (GPT), cholinesterase, glutamate oxaloacetate transaminase (GOT), gamma-glutamyl transpeptidase (gamma-GTP), triglyceride, total cholesterol, uric acid, HbA1c and glucose were significantly higher, and a serum level of HDL-cholesterol was significantly lower in males with fatty liver than in controls with obesity. Prevalence of abnormal laboratory findings in fatty liver was also shown, and prevalence of fatty liver was prominently high in males with severe obesity or with mild elevation of GPT. A major cause of fatty liver was considered as obesity. In conclusion, fatty liver was a common cause of liver dysfunction and was closely related to risk factors for atherosclerosis especially in white-collar workers.
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PMID:[Ultrasonic and laboratory studies on fatty liver in white-collar workers]. 764 60

We developed a sensitive enzyme-linked immunosorbent assay (ELISA) for serum ornithine carbamoyltransferase (OCT) protein, and examined serum OCT concentrations in patients with various liver diseases. OCT concentrations were markedly elevated in cases of hepatic encephalopathy, 'acute on chronic', and those with the acute phase of acute hepatitis, moderately in chronic hepatitis, liver cirrhosis, hepatocellular carcinoma, primary biliary cirrhosis, and slightly in those with a fatty liver. High percentages (92-98%) of patients with chronic hepatitis, liver cirrhosis and hepatocellular carcinoma had higher than normal concentrations of serum OCT protein. There was a close correlation with aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities and moderate correlations with those of mitochondrial AST, glutamate dehydrogenase and gamma-glutamyltranspeptidase. The OCT/ALT ratio was higher in patients with liver cirrhosis than in those with chronic hepatitis (p < 0.001), and was still higher in cases of hepatocellular carcinoma (p < 0.05). In 2 patients with 'acute on chronic' disease, OCT concentrations decreased similarly with or more rapidly than AST or ALT activities after admission. In 2 patients with hepatic encephalopathy, the OCT concentrations changed similarly with AST and ALT activities. This OCT ELISA system will aid in diagnosing various liver diseases and in the follow-up of the patients, and the OCT/ALT ratio may serve for a differential diagnosis of liver diseases.
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PMID:Clinical evaluation of serum ornithine carbamoyltransferase by enzyme-linked immunosorbent assay in patients with liver diseases. 778 67

It is well recognized that consumption of alcohol leads to liver disease in a dose-dependent manner; however, the exact mechanisms remain unclear. Hypoxia subsequent to a hypermetabolic state may be involved; therefore, when it was observed recently that inactivation of Kupffer cells prevented stimulation of hepatic oxygen uptake by alcohol, the idea that Kupffer cells participate in early events that ultimately lead to alcohol-induced liver disease became a real possibility. The purpose of this study was to test that hypothesis. Male Wistar rats were exposed to ethanol continuously by means of intragastric feeding for up to 4 weeks using the model developed by Tsukamoto and French. In this model, ethanol causes fatty liver, necrosis and inflammation--changes characteristic of alcohol-induced liver disease in human beings. Kupffer cells were inactivated by twice weekly treatment with gadolinium chloride (GdCl3), a selective Kupffer cell toxicant. AST levels were elevated to 192 +/- 13 and 244 +/- 56 IU/L in rats exposed to ethanol for 2 and 4 wk, respectively (control value, 88 +/- 7). This injury was prevented almost completely by GdCl3 treatment. Fatty changes, inflammation and necrosis were also all reduced dramatically by GdCl3 treatment. The average hepatic pathological score of rats treated with ethanol for 4 wk was 4.3 +/- 0.6, which was reduced significantly in ethanol- and GdCl3-treated rats to 1.8 +/- 0.5 (p < 0.05). Rates of ethanol elimination were elevated 2- to 3-fold in rats exposed to ethanol for 2 to 4 wk. This elevation was blocked by GdCl3 treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inactivation of Kupffer cells prevents early alcohol-induced liver injury. 804 7

Almost all patients who undergo palatine tonsillectomy for chronic tonsillitis and/or tonsillar hypertrophy manifest postoperative changes in their condition and laboratory data. In some patients, high preoperative transaminase levels decrease postoperatively. I studied 17 patients who had abnormal serum transaminase levels 10 days before tonsillectomy. Before tonsillectomy, serum glutamate oxaloacetate transaminase (GOT) levels were abnormal in half and serum glutamate pyruvate transaminase (GPT) were abnormal in all. Before operation, laboratory values of serum GPT were higher than those of serum GOT in all 17 patients. After tonsillectomy, the abnormal GOT levels in all patients gradually improved to the normal range before the 11th postoperative day and GPT levels did so before the 25th day. Measurement of intracellular transaminase activity of the palatine tonsil suggested that the migration of intracellular transaminase from tonsillar cells to serum would not elevate the serum transaminase level. Postoperative changes in serum transaminase and serum cholinesterase were different from the recovery process observed in fatty liver. The high transaminase level observed in patients with tonsillectomy is suspected to be due to other organs, rather than continuous inflammation of the palatine tonsil.
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PMID:[Changes in transaminase before and after tonsillectomy]. 836 4

Kupffer cells have been implicated in mechanisms of pathophysiology following liver transplantation. Recently, postoperative injury in ethanol-induced fatty liver has been evaluated because fatty livers often fail following transplantation. The low-flow, reflow liver perfusion model was used to study the role of Kupffer cells (KC) in reperfusion injury to fatty livers from rats fed a diet containing ethanol for 4-5 weeks. Treatment with GdCl3, which selectively destroys KC, decreased cell death significantly. Thus, destruction of KC minimized hepatic reperfusion injury, most likely by inhibiting free radical formation and improving microcirculation. Since it was demonstrated recently that destruction of KC prevented the hypermetabolic state observed with acute alcohol exposure, their involvement in events leading to alcohol-induced liver disease was investigated. In rats exposed to ethanol continuously via intragastric feeding for up to 4 weeks, GdCl3 treatment prevented elevation of aspartate aminotransferase (AST) and dramatically reduced the average hepatic pathological score. These results indicate that KC participate in the early phases of alcohol-induced liver injury. Endotoxaemia occurs in alcoholics and activates KC; therefore, we evaluated the effect of minimizing bacterial endotoxin by intestinal sterilization with the antibiotics polymyxin B and neomycin. Antibiotics diminished plasma endotoxin levels significantly and prevented ethanol-induced increases in AST values. These results indicate that endotoxin is involved in the mechanism of ethanol-induced liver injury. A six-line radical spectrum was detected with electron paramagnetic resonance spectroscopy in bile from alcohol-treated rats which was blocked by GdCl3. The free radical adducts had hyperfine coupling constants characteristic of lipid-derived free radical products. In conclusion, these studies demonstrate that KC are involved in reperfusion injury to ethanol-induced fatty livers and hepatic injury due to long-term treatment with ethanol.
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PMID:Role of Kupffer cells in failure of fatty livers following liver transplantation and alcoholic liver injury. 858 36

Non-alcohol-induced steatohepatitis (NASH) is characterized by elevated serum aminotransferase activities with hepatic steatosis, inflammation, and occasionally fibrosis that may progress to cirrhosis. No established treatment exists for this potentially serious disorder. Our aim was to conduct a pilot study to evaluate the safety and estimate the efficacy of ursodeoxycholic acid (UDCA) and clofibrate in the treatment of NASH. Forty patients were diagnosed with NASH based on a compatible liver biopsy with other causes of liver disease, including alcohol abuse, excluded by history, serum tests, and use of ultrasound. Twenty-four patients received 13 to 15 mg/kg/d of UDCA for 12 months. Sixteen patients with hypertriglyceridemia were placed on clofibrate, 2 g/day for 12 months. Twenty-five women and 15 men entered the study. Six of 40 patients (15%) withdrew because of side effects. Four additional patients were withdrawn because of noncompliance; one of them later required liver transplantation. In the UDCA group, the decreases in mean serum levels of alkaline phosphatase, alanine transaminase (ALT), and gamma-glutamyl transpeptidase (GGT) as well as histological grade of steatosis were significant. Among the patients treated with clofibrate, no change from baseline was found in mean ALT, aspartate transaminase (AST), GGT, bilirubin, triglycerides, and cholesterol, or in histological grade of steatosis, inflammation, or fibrosis after 12 months of treatment as compared with entry. Alkaline phosphatase activities decreased significantly from baseline. Despite the known lipid-lowering effects of clofibrate, it did not appear to be of clinical benefit in the treatment of NASH in this 1-year pilot study. However, treatment of NASH with UDCA for 12 months resulted in significant improvement in alkaline phosphatase, ALT, GGT, and hepatic steatosis. The possible benefit of UDCA therapy should be further investigated in the context of a randomized, controlled trial.
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PMID:Ursodeoxycholic acid or clofibrate in the treatment of non-alcohol-induced steatohepatitis: a pilot study. 867 65


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