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

Circulating hormone and metabolite profiles have been studied in ten patients with alcoholic cirrhosis, five patients with alcoholic hepatitis and/or fatty liver, and nine normal controls over a 12-h period of meals and activity. Blood glucose was elevated throughout the day in both cirrhotic and non-cirrhotic alcoholics (mean 12-h glucose; controls 5.38 +/- 0.16 (SEM) mmol/l; cirrhotics 6.98 +/- 0.30 mmol/l, P less than 0.001; non-cirrhotics 7.18 +/- 0.26 mmol/l, P less than 0.001). Non-cirrhotic alcoholics had an exaggerated insulin response to meals, whereas cirrhotic patients had hyperinsulinaemia throughout the day (mean 12-h insulin; controls 16.3 +/- 2.3 mU/l; cirrhotics 35.8 +/- 6.6 mU/l, P less than 0.02). Growth hormone levels were elevated only in patients with cirrhosis (mean 12-h growth hormone, 7.06 +/- 1.35 v. 0.85 +/- 0.17 micrograms/l, P less than 0.001). Serum cortisol was persistently elevated in cirrhotics but only in the evening in non-cirrhotic alcoholics. Lactate and pyruvate responses to meals were exaggerated in non-cirrhotic patients whereas in cirrhotics, levels were persistently raised. Blood glycerol was elevated in all alcoholic patients whereas ketone body levels were normal. Hypertriglyceridaemia was observed only in non-cirrhotic patients. No relationship between the endocrine and metabolic state was observed in either cirrhotic or non-cirrhotic patients.
 ...
PMID:Hormone and metabolite profiles in alcoholic liver disease. 641 54

An experiment was undertaken to investigate the effects of a continuous infusion of catecholamines on glucose and fat metabolism as well as on nitrogen balance and the amount of triglycerides in the rat liver. The animals were nourished by total parenteral nutrition for 5 days and divided into six groups (n = 5 in each group) on the basis of nonprotein calories given with or without an infusion of catecholamines: group G received 100% of nonprotein calories with glucose, group F received 50% of nonprotein calories with glucose, and the remaining 50% with lipid emulsion, groups Epi-G and Epi-F received epinephrine (1 microgram/kg body weight/min) in addition to the same total parenteral nutrition solution as group G or F, and groups Nor-G and Nor-F received norepinephrine (1 microgram/kg/min) in a similar manner. Each group was administered the same number of total calories (252 cal/kg/day) and the same amount of nitrogen (1.49 g/kg/day). Nitrogen balance was better in group G than in group F. Under catecholamine infusion, there were no significant differences in nitrogen balance between groups Epi-G, Nor-G, Epi-F, and Nor-F, but this parameter improved significantly in group Nor-F in comparison to group F. Liver triglycerides was higher in groups Epi-G and Nor-G than in groups Epi-F and Nor-F. Liver triglycerides was directly related to the blood sugar level. These results indicate that nitrogen conservation is improved with lipid emulsion and that glucose rather than lipid plays a significant role in the genesis of fatty liver, when they are administered under catecholamine-induced stress.
 ...
PMID:Effects of exogenous catecholamines on glucose and fat metabolism and on triglycerides in the rat liver during total parenteral nutrition. 643 Nov 31

Earlier studies showed that the fatty liver, caused by feeding rats the Lieber-DeCarli alcohol diet for four weeks, was prevented if the diet was supplemented with dihydroxyacetone (22 g/l), pyruvate (22 g/l) and riboflavin (2.2 g/l). In the present study, we observed that fatty liver was prevented if the alcohol diet was supplemented with glycerol and lactate (22 g/l each) and riboflavin (2.2 g/l). Hence, the prevention of alcoholic fatty liver by the dietary supplementation with dihydroxyacetone and pyruvate may not be related to their capacity to serve as hydrogen acceptors and to oxidize NADH produced during ethanol metabolism. When rats were fed the alcohol diet supplemented with either glycerol or pyruvate, the hepatic triglyceride (TG) levels were similar to those in rats pair-fed a Lieber-DeCarli control diet in which alcohol was replaced with an isocaloric amount of dextrins. Therefore, the prevention of fatty liver does not require the simultaneous presence of several supplements. Dietary dihydroxyacetone or riboflavin did not reduce alcoholic fatty liver. Supplementation of the ethanol diet with isocaloric amounts of lactate or glucose, instead of pyruvate, did not abolish the development of fatty liver but caused a marked reduction in the hepatic TG levels. Animals fed the alcohol diet consumed only small amounts of carbohydrate for long periods of time. Since the inclusion of glucose or its metabolites in the alcohol diet fed to rats caused a marked decrease in the liver TG content, it is likely that the production or prevention of fatty liver is related to carbohydrate metabolism.
 ...
PMID:Fatty liver caused by chronic alcohol ingestion is prevented by dietary supplementation with pyruvate or glycerol. 648 82

The progression of neurological abnormalities through four or five clinically distinguishable levels of deepening coma and the development of a fatty liver are the hallmarks of Reye syndrome. A number of animal models have been described that result in fatty liver formation with minimal, static, or catastrophic neurological changes. In this study, we attempted to produce neurological features in rabbits that reflected a rostral-caudal progression of abnormalities that could be categorized into clinically distinguishable levels reminiscent of Reye syndrome. This was accomplished by the intracisternal administration of 0.5-25 mg of 11,14-icosadienoic acid (20:2 omega 6) suspended in a mixture of rabbit serum and isotonic saline solution. A reproducible, dose-titratable spectrum of at least four levels of deepening coma could be produced at will. Increases in serum glutamate-oxaloacetate transaminase and creatine kinase and changes in serum glucose resulted 1-2 hr after the neurological abnormalities were evoked. Other unsaturated fatty acids produced similar responses. Those tested included 18:1 omega 9, 18:2 omega 6, 18:3 omega 3, 20:3 omega 6, 20:4 omega 6, and 22:4 omega 6 fatty acids. Saturated fatty acids, including 6:0, 8:0, 16:0, 18:0, and 20:0, failed to elicit these effects. The abnormalities were sustained for 30-120 min after a single dose. Full recovery was observed in some animals that had not reached the fourth level of our grading system for coma. Pretreatment of the rabbits with aspirin modulated the neurological abnormalities. Twenty micrograms of bee venom melittin, which activates endogenous phospholipase A2, administered intracisternally into rabbits also produced signs of level 3 (our grading system) coma for several hours. These findings suggest a possible role for polyunsaturated fatty acids in the development of Reye syndrome and offer a means of producing the neurological components of that syndrome in a laboratory animal.
 ...
PMID:Development of encephalopathic features similar to Reye syndrome in rabbits. 659 8

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.
 ...
PMID:Fatty liver and kidney syndrome in chickens as an animal model for Reye's syndrome. 664 49

The purpose of this study was to ascertain 1) fatty infiltration of the liver in spontaneously ketotic cows and 2) the most appropriate blood components to aid diagnosis of ketotic fatty liver. Liver biopsies and blood samples were obtained under field conditions. Cows were divided into three groups (healthy, mildly ketotic, and severely ketotic) by their blood ketone body concentrations. Severely ketotic cows had a greater percent fat in the liver than healthy cows. The mildly ketotic group fell between the other two groups and was significantly different from only the severely ketotic group. There was a positive correlation between fatty infiltration and blood ketone body concentrations but a negative correlation with glucose concentrations. Liver-specific enzymes were positively correlated with fatty infiltration. Only ornithine carbamoyltransferase and iditol (sorbitol) dehydrogenase could be used to separate healthy cows from those with severe ketosis. The best equation to explain the variation of percent fat in liver included concentration of beta-hydroxybutyrate (BHB) and logarithm of ornithine carbamoyltransferase concentration (Log-OCT): % Fat = -6.15 + 2.39 (BHB) + 11.7 (LogOCT) Although this equation explained 39.5% of the variation, it could not be used to predict reliably percent fat in the liver. Liver biopsy seems still to be the only reliable method of measuring of fatty infiltration in the liver.
 ...
PMID:Fatty infiltration of liver in spontaneously ketotic dairy cows. 665 90

Cows from three different herds were used to investigate the relationship between plasma D(-)-3-hydroxybutyrate, serum free fatty acid and blood glucose concentrations and the amount of fat present in the liver in the week after calving. The study was particularly concerned with the diagnostic value of D(-)-3-hydroxybutyrate estimations. These estimations did not make a significant contribution to diagnosis of fatty liver nor did they reflect accurately the nutritional status of the cows.
 ...
PMID:Blood composition and liver fat in post parturient dairy cows. 668 51

Ten cases of fatty liver of pregnancy are reported from a large metropolitan medical center for the period 1972 to 1982. Compared to earlier reports, a marked decrease in both maternal and fetal mortality was noted (1 mother died and 2 of 12 infants were stillborn). Eight other cases obtained from liver biopsies referred from other hospitals were also reviewed and combined mortality data were similar. Since delivery was spontaneous in 8 of our 10 patients, the lower mortality cannot be attributed to early delivery. Instead, we ascribe it to improved supportive therapy with transfusions, clotting factors, antibiotics, glucose and monitoring. Also, earlier reports emphasized autopsy material. The incidence of FLP was 1 per 13,328 deliveries in a predominantly Hispanic population. Our review yielded new data concerning presenting signs and symptoms, laboratory features including serial clotting screens documenting disseminated intravascular coagulation (DIC), obstetric and perinatal information as well as maternal follow-up.
 ...
PMID:Idiopathic fatty liver of pregnancy: findings in ten cases. 669 Aug 83

Blood glucose, serum insulin, C-peptide, free fatty acids and growth hormone were evaluated in 45 patients with histologically established hepatic steatosis after an oral glucose load (100 g). Glucose tolerance was impaired in 59 per cent of the patients. Significantly increased levels were found for blood glucose (fasting and after 60 and 120 min), insulin (after 60, 120 and 180 min), C-peptide (fasting and after 60, 120 and 180 min), and free fatty acids (fasting and after 60 and 120 min). Human growth hormone levels were not altered. After glucose administration the C-peptide/insulin ratio was significantly reduced in hepatic steatosis compared to controls. In patients with hepatic steatosis there were no differences between subjects with normal body weight or overweight nor between stadium I and stadium II ('alcoholic hepatic steatosis') concerning glucose, insulin, C-peptide, HGH and FFA levels in blood. We conclude, that hepatic steatosis is associated with relative insulin resistance to which elevated FFA may contribute. In addition, the decreased C-peptide/insulin ratios suggest an impaired hepatic insulin degradation as it was already described for more serious liver diseases.
 ...
PMID:Hyperinsulinemia in hepatic steatosis. 674 19

Studies were made on whether glucose starvation causes fatty liver in pyridoxine-deficient male Wistar rats. Pyridoxine deficiency resulted in significantly lower levels of liver glucose than in pair-fed controls but no significant change in the serum glucose concentration. In non-starving animals, serum immuno-reactive insulin (IRI) was significantly lower in pyridoxine-deficient rats than in pair- or ad libitum-fed controls. Liver glucokinase activity in pyridoxine-deficient rats was also significantly lower than in ad libitum-fed controls. The extent of insulin deficiency was evaluated by examining the effect of administration of insulin on pyridoxine-deficient rats. Administration of insulin had no effect on the activity of liver glucokinase in pyridoxine-deficient rats, but induced the enzyme in ad libitum-fed controls. In response to a decrease in the activity of liver glucokinase or hexokinase in the deficient group, glycolytic activity, estimated as lactate production from glucose in the liver supernatant spun at 100,000 X g, was reduced to half the control level in pyridoxine-deficient rats. The effects of glucose administration on the liver lipid content, serum insulin and serum glucose were investigated. The serum glucose concentration was not significantly different in pyridoxine-deficient and control rats at any time after the glucose load. The level of serum IRI after the load was similar in the two groups after 30 min but then gradually decreased in the deficient group. The liver lipid content of the deficient rats tended to decrease whereas that of the controls remained unchanged throughout the experiment. Thus glucose starvation in pyridoxine-deficient rats is one factor responsible for fatty liver formation. Possible mechanisms of this phenomenon are discussed.
 ...
PMID:Role of glucose on fatty liver formation in pyridoxine-deficient rats. 675 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>