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PubMed2001

Relationship between serum TNF activity and insulin resistance in dairy cows affected with naturally occurring fatty liver.

To clarity the relationship between tumor necrosis factor (TNF) and insulin resistance in dairy cows affected with fatty liver, naturally occurring cases were investigated. The affected cows were classified into following three groups according to histopathologic findings of the liver: mild fat droplet deposition (group 1; n=11), severe fat droplet deposition (group 2; n=10), and cloudy swelling (group 3; n=8). Serum TNF activities in Group 2 (8.67 +/- 2.16 U/ml) and Group 3 (11.65 +/- 1.92 U/ml) were significantly higher than that in Group 1 (3.57 +/- 0.81 U/ml) (p<0.05). The insulin-tolerance tests showed that the insulin-stimulated glucose disposal rates (GDR) in Group 2 (27.6 +/- 7.8%) and Group 3 (15.8 +/- 9.1%) were significantly lower than that in Group 1 (41.7 +/- 9.8%). There was a significant negative correlation between serum TNF activity and GDR in affected cows (r=-0.56, p<0.01). These results indicate that serum TNF activity is correlated with insulin resistance in cows with fatty liver.

Animals↗
PubMed2002

[Acute fatty liver in pregnancy: clinical and histopathological course. Case report].

Acute fatty liver of pregnancy is a rare disease which may be letal if diagnosis is missed. The pathogenesis is not completely clear, but there is some evidence that some cases have been associated with a genetic deficiency of fatty acid beta-oxidation. Other predisposing factors include primiparity, multiple pregnancy, male fetal sex and pre-eclampsia. Clinical presentation and laboratory findings are often unspecific. Increasing serum aminotransferases are characteristic in the early stage of the disease. Liver biopsy establishes the diagnosis and typically shows microvesicular, centrilobular fatty changes of hepatocytes. Differential diagnosis includes the HELLP-Syndrome, cholestasis of pregnancy, pre-eclampsia and viral or drug induced hepatitis. Without adequate treatment liver failure with coagulopathy and encephalopathy may develop. Two cases of acute fatty liver in pregnancy in an early stage are presented. Clinical and histopathological findings as well as diagnostic and therapeutic procedures are discussed.

Adult↗
PubMed1981

Tetracycline-associated fatty liver of pregnancy, including possible pregnancy risk after chronic dermatologic use of tetracycline.

Two cases of tetracycline-associated fatty liver of pregnancy are reported. In one, the history was negative for antibiotic use, yet autopsy revealed typical gross and microscopic bone fluorescence of tetracycline. Tissue extraction and chemical analysis showed qualitative evidence of tetracycline, whereas quantitation revealed 60 microgram/gm of wet bone tissue. Findings in our cases and in those from the literature indicate that the association of tetracycline use and fatty liver of pregnancy is even more common than has been suggested.

Adult↗
PubMed2006

Nonalcoholic fatty liver disease and HIV infection.

As persons with HIV live longer, chronic liver disease is increasingly important. Nonalcoholic fatty liver disease (NAFLD) is characterized by excess fat in hepatocytes in patients without significant alcohol use. It can progress from steatosis to nonalcoholic steatohepatitis (NASH) to cirrhosis. Visceral obesity and insulin resistance are integral to the pathogenesis of NAFLD. Patients with HIV are at greater risk of NAFLD due to antiretroviral therapy and viral hepatitis coinfection. Antiretroviral therapy can lead to patterns of injury that include steatosis and NASH. Coinfection with hepatitis C virus increases the risk of insulin resistance and hepatic steatosis, and co-existent features of NASH have also been reported. Histological-based, longitudinal studies are needed that address the interactions of NAFLD and HIV infection, the effects of antiretroviral therapy and hepatotropic virus coinfection, and inform better management strategies.

Fatty Liver↗
PubMed1990

Microvesicular fatty liver in rats with resembling Reye's syndrome induced by 4-pentenoic acid.

To produce an animal model of Reye's syndrome (RS), 20 adult male Wistar rats were given 10 repeated i.p. injections of 50 mg/kg 4-pentenoic acid (PA) each separated by an 8-h interval. Then, 90 min after the tenth dose, they were given a final i.p. injection of 150 mg/kg PA. Thirteen control animals were injected with vehicle only using the same time schedule. More than half the animals in each group were fed a common diet, but the others were fasted during the terminal 10-h stage. All rats were sacrificed 30 min after the last injection. At the terminal stage, in comparison with the vehicle-injected controls, hypolipemia, hypoglycemia and high titers of serum ammonia and urea N were estimated significantly in the PA-treated rats fed throughout the whole period. Hypolipemia and hypoglycemia were more prominent in the terminally fasted group than the group fed continuously. Only in the PA-treated rats fed throughout the whole period moderate morphological signs of microvesicular fatty liver were exhibited. Ultracytochemical findings and biochemical determinations showed that the major lipids in the microvesicular fatty livers were triglycerides. Morphometric analysis revealed distinct hepatic mitochondrial swelling in the PA-treated rats. Therefore, the above treatment with PA was able to induce microvesicular fatty liver in rats with resembling RS, which were fed throughout the treatment procedure, but not in the terminally fasted rats.

Animals↗
PubMed1990

Peripheral bone mineral content in patients with fatty liver and hepatic cirrhosis.

The aim of our study was to determine peripheral bone mineral content (BMC) and serum osteocalcin (OC) levels in two groups of patients with fatty liver and hepatic cirrhosis as compared with a control group comprising healthy subjects. Group I consisted of 18 male patients (mean age, 51 years) with hepatic steatosis, group II included 23 men (mean age, 52 years) with hepatic cirrhosis. In all patients diagnosis was established with ultrasonic examination of the liver; 18 patients in group II underwent additional blind liver biopsies. The control group consisted of 23 subjects. Analysis of variance showed marked differences between the three groups (p less than 0.001). Peripheral BMC was significantly lower in patients with liver cirrhosis (BMC, 46.8 U) than in both patients with fatty liver (BMC, 54.7 U) and the control group (BMC, 60.7 U). However, no statistically significant differences in BMC values occurred between patients with hepatic steatosis and the controls. Serum osteocalcin levels followed a pattern similar to that of BMC values. A statistically significant decrease in osteocalcin values was found in the liver cirrhosis group (OC, 3.9 ng/ml) compared with the control group (OC, 6.6 ng/ml) and with the patients with hepatic steatosis (OC, 6.2 ng/ml). According to these results, clearly reduced BMC and decreased OC levels are found in patients with chronic alcoholic liver disease. However, these reductions are essentially influenced by the extent of morphologic changes in liver structure.

Adult↗
PubMed1994

On the molecular origin of charge heterogeneity of rat liver fatty acid-binding protein (Z-protein).

The occurrence of many charge isoforms is known for rat liver fatty acid-binding protein, and this is the major cause of conflicting data on the characterization of the protein. Recently, M. Li and T. Ishibashi (1992, Arch. Biochem. Biophys. 298, 254-258) clearly demonstrated that some charge isoforms are due to bound fatty acids. We found that acidic fraction (DE-III) of rat liver fatty acid-binding protein contained isoaspartyl-105 protein resulted from deamidation and peptide rearrangement at Asn-105. Since DE-III fraction carries mainly arachidonate, this post-translational modification might modulate binding specificity of fatty acid-binding protein.

Amino Acid Sequence↗
PubMedDate not supplied

[Acute fatty liver of pregnancy].

Liver diseases in pregnancy can occur as a complication of gestation or independently. Acute fatty liver of pregnancy is a rare disease of unknown etiology specifically associated to gestation. The frequency is increased in the first pregnancy, in the last trimester and in multiple pregnancies. Because of the high maternal and perinatal mortality early diagnosis is necessary for prompt termination of pregnancy. This case report is intended to facilitate the differentiation between acute fatty liver of pregnancy and other liver diseases in pregnancy. The differential diagnoses include preeclampsia, HELLP syndrome, intrahepatic cholestasis of pregnancy and acute viral hepatitis.

Acute Disease↗
PubMed2004

A novel aminosterol reverses diabetes and fatty liver disease in obese mice.

BACKGROUND/AIMS: Non-alcoholic fatty liver disease (NAFLD) is common in obesity. However, weight reduction alone does not prevent the development or progression of NAFLD. Since NAFLD is associated with insulin resistance and diabetes, we hypothesized that improvement of these factors would reverse obesity-related NAFLD. METHODS: We examined the effects of an aminosterol, 1436, on glucose, lipids and liver metabolism in Lep(ob/ob) mice, a model of obesity, severe insulin resistance, diabetes, hyperlipidemia and hepatic steatosis. RESULTS: 1436 decreased body weight, specifically fat content, by inhibiting food intake and increasing energy expenditure. In contrast to weight loss from food restriction, this aminosterol specifically lowered circulating lipids, reversed hepatic steatosis and normalized alanine aminotransferase level. 1436 decreased glucose, increased adiponectin and enhanced insulin action in liver. These changes culminated in inhibition of hepatic triglyceride synthesis and increased fatty acid oxidation. Gene expression studies confirmed a reduction in lipogenic enzymes in liver, and elevation of enzymes involved in lipid catabolism. CONCLUSIONS: These results demonstrate that 1436 is an effective treatment for insulin resistance and hepatic steatosis in Lep(ob/ob) mice, by decreasing hepatic lipid synthesis and stimulating lipolysis. In contrast, weight loss from food restriction has no substantial effect on insulin resistance, lipids and hepatic steatosis.

Animals↗
PubMed1985

Isolation, purification, and characterization of a peptide that contains the beta-ketoacyl reductase, enoyl reductase, and beta-hydroxyacyl dehydrase activities of the pigeon liver fatty acid synthetase.

Controlled proteolytic cleavage of pigeon liver fatty acid synthetase with elastase (4% w/w) for 5 h yields two peptides that are designated II and IV. After 5 h of proteolysis the incubation mixture containing these peptides retains all of the component enzyme activities of the fatty acid synthetase complex. The two peptides are then separated by chromatography on an Affi-Gel Blue column. Gel filtration of the fraction containing peptide II yields a homogeneous peptide as shown by polyacrylamide gel electrophoresis in the presence and absence of sodium dodecyl sulfate. The molecular weight of this peptide has been estimated to be 130 000 by sodium dodecyl sulfate--polyacrylamide gel electrophoresis, size exclusion chromatography, and amino acid analysis. The sedimentation coefficient for peptide II is approximately 7.4S. Peptide II contains the domains for the beta-ketoacyl and enoyl reductases and beta-hydroxyacyl dehydrase activities of the fatty acid synthetase complex.

3-Oxoacyl-(Acyl-Carrier-Protein) Reductase↗
PubMed1998

Preventive effects of dehydroepiandrosterone acetate on the fatty liver induced by orotic acid in male rats.

Preventive effects of dehydroepiandrosteone acetate (DHEA-A) and clofibrate (positive control substance) on the fatty liver induced by orotic acid (OA) were examined on the male Sprague-Dawley rats fed a high sucrose based diet containing 1% OA and this diet further mixed with 0.5% DHEA-A or 0.5% clofibrate for 2 weeks. Numerous lipid droplets were observed in the hepatocytes of the rats treated with OA alone, but not in those treated with DHEA-A or clofibrate. In comparison to the group with OA alone, the DHEA-A or clofibrate treated rats showed a larger relative liver weight (to body weight) which was accompanied by increased peroxisomes in the hepatocytes. These results indicate that DHEA-A, as well as clofibrate, may prevent OA-induced fatty liver.

Animals↗
PubMed2001

Acute fatty liver of pregnancy associated with short-chain acyl-coenzyme A dehydrogenase deficiency.

There is a correlation between pregnancy complications such as acute fatty liver of pregnancy and long-chain 3-hydroxyacyl-coenzyme A dehydrogenase (LCHAD) deficiency. We diagnosed another fatty acid beta-oxidation defect, short-chain acyl-coenzyme A dehydrogenase deficiency, in an infant when evaluating him because his mother had acute fatty liver of pregnancy. Other beta-oxidation defects, in addition to LCHAD deficiency, should be considered in children born after pregnancies complicated by liver disease.

Adult↗
PubMed1992

The binding of the fluorescent ATP analogue 2'(3')-trinitrophenyladenosine-5'-triphosphate to rat liver fatty acid-binding protein.

The less polar fluorescent analogue of ATP, 2'(3')-trinitrophenyl-5'-triphosphate bound to rat liver fatty acid-binding protein with high affinity (Kd 6.3 x 10(-6) M) and 1:1 molar stoichiometry. This probe bound to the fatty acid binding site of the protein and was displaced by oleic acid and oleoyl CoA. High concentrations of ATP did not cause significant displacement of the fluorescent ATP analogue. Since the anionic part of this molecule is the triphosphate group it is difficult to envisage this group being accommodated at an anion binding site within the non-polar core of this protein as is the case with other fatty acid binding proteins. Therefore it is anticipated that the ligand must bind to liver fatty acid-binding protein with this triphosphate group surface exposed. Caution must be exercised when using the more hydrophobic fluorescent analogue of ATP to investigate the ATP binding properties of proteins.

Adenosine Triphosphate↗
PubMed2005

Up-regulation of ADRP in fatty liver in human and liver steatosis in mice fed with high fat diet.

The present study was performed to examine a role of adipose differentiation-related protein (ADRP) in the process of liver steatosis. Immunohistochemical findings indicated that ADRP expression is increased in the hepatocytes in patients with fatty liver when compared with normal liver. ADRP expression is localized in the surface of lipid droplets in the hepatocytes. Increased expression of ADRP mRNA and protein was similarly observed in fatty liver in ob/ob mice and the liver steatosis induced by high fat diet in mice. The up-regulation of ADRP mRNA and protein in the liver by high fat diet was identified in the surface of lipid droplets in a time-dependent manner. Recent studies demonstrated that up-regulation of PPARgamma in the hepatocytes is deeply involved in liver steatosis. To clarify whether ADRP expression is increased by PPARgamma activation in hepatocytes, we examined the effect of a PPARgamma ligand, troglitazone, on ADRP mRNA expression in HepG2 cells. ADRP mRNA expression was increased by troglitazone in dose- and time-dependent manners. All these results suggest that ADRP is up-regulated in liver steatosis in human and mice, and that high fat diet increases expression of ADRP through PPARgamma activation, followed by induction of liver steatosis.

Animals↗
PubMedDate not supplied

Efficacy of omega-3 fatty acids, atorvastatin and orlistat in non-alcoholic fatty liver disease with dyslipidemia.

AIM: To evaluate the efficacy and safety of three hypolipidemic agents in patients with non-alcoholic fatty liver disease associated with hyperlipidemia. METHODS: Patients with dyslipidemia (Fredrickson type IIb), asymptomatic persistent transaminasemia lasting 24 weeks, and evidence of hepatic fat infiltration on ultrasonography and liver biopsy were studied. Those with predominant hypertriglyceridemia received omega-3 fatty acids (5 mL thrice daily) (Group A), those with predominant hypercholesterolemia received atorvastatin 20 mg/daily (Group B), and overweight patients received orlistat 120 mg thrice daily before meals (Group C). After 24 weeks of treatment, serum transaminase and lipid levels and liver ultrasonography were repeated. RESULTS: Serum transaminase levels decreased significantly (p< 0.001) in all groups but the decrease was more marked in Group C (AST 75 [16] to 31 [7] IU/L; ALT 120 [38] to 41 [10] IU/L) than in Group A (AST 70 [14] to 41 [6]; ALT 110 [20] to 68 [12]) or Group B (AST 68 [13] to 46 [9]; ALT 115 [22] to 76.6 [13]). After treatment, ultrasonography showed resolution of fatty liver in 35% of patients in Group A, 61% in Group B, and in 86% in Group C (p< 0.001, Group C vs. A). CONCLUSIONS: A decline in transaminase levels and normalization of ultrasonographic evidence of fatty liver were observed on treatment with omega-3 fatty acids in patients with hypertriglyceridemia, with atorvastatin in those with hypercholesterolemia, and orlistat in overweight patients with hyperlipidemia.

Adult↗
PubMed1983

Serum prealbumin, transferrin and immunoglobulins in fatty liver, alcoholic cirrhosis and primary biliary cirrhosis.

The serum concentrations of prealbumin, transferrin and immunoglobulins, as well as their concentration ratios, were determined in patients with fatty liver, alcoholic cirrhosis and primary biliary cirrhosis to evaluate the usefulness of these measurements in the differentiation between these diseases, and in the evaluation of the severity of the liver injury. Alcoholic cirrhosis was characterized by high IgA/prealbumin and IgG/prealbumin ratios, whereas in fatty liver these ratios remained normal or close to normal. The IgG concentration and the ratio of IgG/prealbumin were markedly higher in advanced than in early alcoholic cirrhosis, IgG/prealbumin being the most sensitive indicator. None of the assays reflected the degree of fatty degeneration. In primary biliary cirrhosis the mean IgG concentration was 93% higher than in alcoholic cirrhosis. One of ten patients with primary biliary cirrhosis had a normal IgM level, whereas 2 of 10 patients with alcoholic cirrhosis had a value above normal (greater than 2.9 g/l). IgM alone did not differentiate between alcoholic and primary biliary cirrhosis, while the ratio of IgA/IgM seems useful: a value over 2.0 was found in all patients with alcoholic cirrhosis but in none of those with primary biliary cirrhosis.

Adult↗
PubMed1986

A role of the heavy subfraction of the floating lipids in acute alcoholic fatty liver of rats.

Two subfractions of floating lipids were studied to clarify the subcellular pathogenesis of ethanol-induced acute fatty liver in the rat. The main lipid in both the heavy and light subfraction was triglyceride, but the heavy subfraction was richer in phospholipids than the light subfraction. After ethanol-treatment of the animals, not only triglyceride but also phospholipids increased significantly in the light subfraction. The similarity of the phospholipid species in the two subfractions suggests a possible exchange of lipids between them. The heavy subfraction consisted of membrane-free lipid droplets of very low density lipoprotein (VLDL) size plus membrane-bound, vacuolated organelles; the light subfraction consisted of membrane-free lipid globules larger than 1000 nm in diameter. Occasionally adherent particles, 40 to 100 nm in diameter, were detected on the surface of the lipid globules. After ethanol treatment, the ratio of adherent particles to lipid globules increased significantly. These observations suggest that the biogenesis of acute alcoholic fatty liver in rats involves first the formation of membrane-free lipoproteins of VLDL size in the cytoplasm and subsequently their fusion to pre-existing lipid globules.

Acute Disease↗