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)

Reye syndrome was observed in a 5 1/2-year-old girl after an appendectomy. It was accompanied by insulin-resistant hyperglycaemia. Central adaptation failure resulted in death on the fourth day of treatment. Post mortem and histological results showed phlegmonous pancreatitis of the excretory type, apart from the established manifestations of Reye syndrome (severe cerebral oedema, excessive hepatic steatosis, moderate fatty degeneration of renal tubuli). Neuropathology revealed exclusively signs of hypoxic damage. Pancreatitis, usually necrotising or haemorrhagic, is not infrequent in Reye's syndrome. Girls are predominantly affected and pancreatitis is associated with a tendency towards sometimes serious hyperglycaemia. The possibility of this complication should be considered in the treatment of Reye syndrome.
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PMID:[Reye's syndrome with pancreatitis and hypoxic brain damage]. 669 70

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.
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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.
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PMID:Role of glucose on fatty liver formation in pyridoxine-deficient rats. 675 93

Obesity is often associated with coronary heart disease and metabolic disorders. In this study, the relationship between obesity and metabolic disorders and between obesity and fatty liver by ultrasonography was investigated in 307 university students (18-20 years old, men: 196, women; 111). The correlation between Body Mass Index (BMI) and the thickness of subcutaneous fat (ST) was significant between BMI and the ratio between waist and hip circumference (WHR) was more significant in male students (r = 0.838, p < 0.001) than in female students (r = 0.639, p< 0.001). The incidence of fatty liver was significantly higher in male obese students (68.6%) than in female obese students (27.3%). After adjustment for BMI, ST, WHR and sigma glucose, the mean values for serum transaminase, cholinesterase, total cholesterol, uric acid, fasting plasma insulin and sigma insulin were significantly higher in male obese students with fatty liver than in male obese students without fatty liver. The present study suggested that male obese students with fatty liver are more likely to have metabolic disorders than male obese students without fatty liver.
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PMID:[Fatty liver and obesity in university students]. 747 66

High-calorie total parenteral nutrition (TPN) is associated with hepatic dysfunction and steatosis. Because TPN-induced steatosis might compromise hepatic expression of insulin-like growth factor-I (IGF-I) and thereby limit its potential nutritional benefit, we examined hormonal and IGF-I responses in male Sprague-Dawley rats (270 to 300 g) fed by continuous intravenous infusion with high-calorie, high-dextrose (350 kcal/kg) TPN solutions for O (control), 2, 4, and 8 days. Since IGF-binding proteins (IGFBPs) are thought to modulate the biological effects of IGFs in target tissues, we also determined serum levels of IGFBPs. Animals developed hepatic steatosis after 2 to 8 days of TPN, as reflected by a sevenfold to 15-fold increase in hepatic triacylglycerol content (P < .001 v control on each day). Serum corticosterone and insulin levels were significantly higher after 2 and 4 days of TPN, whereas serum growth hormone levels were reduced after 4 and 8 days. Serum IGF-I levels were not significantly different during TPN. However, there was a coordinate reduction in the three major hepatic IGF-I transcripts (7.0, 1.9, and 1.0 kb) after 2, 4, or 8 days of TPN, and IGF-I transcripts corresponding to multiple initiation sites within exons 1 and 2 were coordinately downregulated with TPN. Western ligand blotting indicated that serum levels of 38K to 43K, 30K to 34K, and 24K IGFBPs were increased approximately twofold after 4 and 8 days of TPN as compared with control values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High-calorie total parenteral nutrition reduces hepatic insulin-like growth factor-I mRNA and alters serum levels of insulin-like growth factor-binding protein-1, -3, -5, and -6 in the rat. 753 78

The presence of hepatic steatosis was determined in 180 middle-aged male workers by ultrasonography and was found in 39 (22%) of them. Body mass index (BMI), systolic and diastolic blood pressure (BP) and serum levels of asparate aminotransferase (AST), alanine aminotransferase (ALT) and gamma-glutamyl transpeptidase (gamma-GTP) were higher in the subjects with hepatic steatosis. Although the volume of alcohol consumed in a week did not differ between the subjects with and without hepatic steatosis, the hepatic steatosis was thought to relate to both increased body mass and alcohol consumption because the elevations of serum AST and gamma-GTP in the subjects depended largely on alcohol consumption but not on BMI. The results of 75 g oral glucose tolerance test showed a higher blood glucose at 120 minutes and a higher plasma immunoreactive insulin at baseline, 60 and 120 minutes in the subjects with hepatic steatosis, being adjusted for age, BMI and alcohol consumption. The significant association between serum gamma-GTP and BP, which had been often observed in alcohol consumers, was no longer significant after adjustment for plasma insulin levels whereas plasma insulin showed a significant association with BP. These results suggest the possibility that hypertension in alcohol consumers, and also in obese people, relates at least partly to hyperinsulinaemia associated with progression in hepatic steatosis.
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PMID:Association between hepatic steatosis, insulin resistance and hyperinsulinaemia as related to hypertension in alcohol consumers and obese people. 775 70

In experimental animals the enhancement of hepatic fatty acid oxidation and ketogenic capacity is accompanied by a rise in the concentration of liver carnitine. Massive obesity is characterized by enhanced fatty acid turnover, insulin resistance, and often a fatty liver. Carnitine concentrations were determined in liver, abdominal muscle tissue, and blood in morbidly obese women. The liver and muscle carnitine concentrations were significantly higher in the obese subjects than in the lean control subjects. These findings suggest an increase of the whole-body carnitine pool. In the obese subjects there was also a significant positive correlation between liver and muscle carnitine concentrations. In the majority of the obese subjects fatty changes could be demonstrated in the liver. The plasma insulin concentration tended to be positively correlated with the degree of fat infiltration and negatively correlated with the liver carnitine content. It is concluded that the liver carnitine content is significantly increased in obese women, which agrees with the finding in experimental animals.
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PMID:Increased liver carnitine content in obese women. 782 32

The mitochondrial FAD-linked enzyme glycerophosphate dehydrogenase plays a key role in the pancreatic B-cell glucose sensing device. In the present study, the activity of this enzyme was examined in islets of fa/fa rats in which inherited diabetes mellitus is associated with obesity, hyperinsulinism and severe insulin resistance. The specific activity of both FAD-linked glycerophosphate dehydrogenase and glutamate dehydrogenase were decreased in islet and liver homogenates prepared from fa/fa, as compared to Fa/Fa, rats, this coinciding with a low ratio between glutamateoxalacetate and glutamate-pyruvate transaminase activity in both islet and liver extracts, islet hyperplasia, hyperinsulinemia and hepatic steatosis in the hyperglycemic fa/fa rats. It is speculated that a low activity of FAD-linked glycerophosphate dehydrogenase in the pancreatic B-cell may participate to the perturbation of glucose homeostasis in fa/fa rats, like in other animal models of non-insulin-dependent diabetes mellitus.
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PMID:Impaired FAD-glycerophosphate dehydrogenase activity in islet and liver homogenates of fa/fa rats. 783 41

This study was designed to test the hypothesis that deprivation of enteral feeding contributes to the development of total parenteral nutrition (TPN)-induced hepatic dysfunction and that alterations of gut hormones are involved in its pathogenesis. Twenty-one adult Sprague-Dawley rats were randomized into three groups: group 1 received chow feeding ad libitum (288 kcal/kg per day); group 2 received dextrose-based TPN (320 +/- 5 kcal/kg per day); and group 3 received TPN (315 +/- 15 kcal/kg per day) plus chow feeding ad libitum (74 +/- 1 kcal/kg per day). After 7 days, portal blood was assayed for insulin, glucagon, gastrin, peptide YY, secretin, and vasoactive intestinal polypeptide; systemic blood for determination of liver function tests and serum lipid analysis. Liver biopsies were taken for histology and staining for fat, and the remainder of the livers were removed for tissue lipid analysis. TPN induced striking hepatic steatosis with prominent histologic changes and accumulation of lipids, mainly triglycerides and cholesterol ester, in the liver. Addition of enteral feeding to TPN-treated animals significantly reduced the histologic changes as well as lipid accumulation in the liver. Portal plasma levels of gastrin and peptide YY were reduced in animals maintained on TPN alone, with no change in secretin or vasoactive intestinal polypeptide levels. Enteral supplementation increased peptide YY levels in group 3, but not to normal, while gastrin secretion remained decreased. The serum triglyceride levels were decreased in both TPN groups; no differences were detected in the serum cholesterol levels or liver function tests.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of enteral feeding on hepatic steatosis induced by total parenteral nutrition. 816 98

We have previously reported that fatty liver is easily induced in a novel experimental animal, Suncus murinus (suncus) by withholding food, and that apolipoprotein B (apo B) is not actively synthesized in the liver. In the present paper we describe the effect of starving and refeeding on lipid and lipoprotein metabolism in suncus, in order to explore the mechanisms of induction of fatty liver by starving and of its improvement by refeeding. Starvation induced increase in triglyceride content and decrease in glycogen content of the liver. Although the glycogen content returned to the level before starvation at 12 h after refeeding, the triglyceride content decreased gradually but did not reach the prestarvation level even at 24 h after refeeding in suncus. Plasma lipids, glucose, and insulin levels were decreased by starvation and returned to the levels before starvation between 8 and 24 h after refeeding. On the other hand, the plasma levels of free fatty acid and ketone bodies were elevated significantly by starvation and decreased rapidly by refeeding. These responses to starvation and refeeding, except for the change in hepatic triglyceride, are in common with other experimental animals, suggesting that there are no abnormalities in glucose metabolism or in fatty acid metabolism in suncus. In conclusion, the fatty liver induced by starvation in suncus may be caused by impaired triglyceride transport out of the liver, for which apolipoprotein B is mostly responsible, as reported previously.
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PMID:Effect of starving and refeeding on lipid metabolism in suncus. 820 66


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