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PubMed1981

Computed tomography attenuation values in fatty liver.

The accuracy of CT diagnosis of increased fat deposition in the liver was assessed in 11 alcoholic patients with suspected fatty liver. Single-energy CT attenuation values were compared with histological assessment of fatty liver and chemical analysis of liver triglyceride concentrations, obtained from liver biopsy specimens. Measured attenuation values showed an inverse correlation with the degree of fatty change assessed histologically (r =--0.90; p Less Than 0.0001) and with that assessed chemically (r=--0.57; p Less Than 0.05). CT scanning may provide a useful non-invasive method for detecting and following patients with fatty liver, particularly when liver biopsy is contraindicated.

Adult↗

PubMed1978

[Attenuation values of normal and pathological liver tissue as a basis for computer tomographic densitometry of fatty livers (author's transl)].

Measurements of the density of normal and diffusely disease liver parenchyma show a significant difference only in the presence of fatty livers. A linear relationship between the fat content and density (g/cm3) has been demonstrated. Computer tomographic densitometry of liver tissue correlates well with physical in vitro measurements and permits measurements of fat content which are sufficiently accurate for clinical use. Other types of liver disease cannot be differentiated by densitometry.

Absorptiometry, Photon↗

PubMed1979

Nutritional and metabolic aspects of fatty liver disease in poultry.

There are two metabolic disorders of major commercial importance in poultry that involve the occurrence of fatty deposits in the liver. Fatty Liver and Kidney Syndrome (FLKS) affects young birds and the main manifestations, lipid infiltrations into liver and many other organs, are apparently secondary effects of the primary lesion that lies in carbohydrate metabolism. Although several nutritional and environmental factors influence FLKS, the main factor is the vitamin, biotin. In the absence of an adequate supply of biotin, the hepatic activity of pyruvate carboxylase, a biotin-dependent enzyme, becomes so low that gluconeogenesis in the liver via pyruvate becomes negligible. When the bird is then subject to a mild stress and/or short term fasting, liver glycogen reserves become rapidly depleted and a progressive hypoglycaemia develops that ultimatley proves fatal. Supplementing diets with adequate amounts of biotin can prevent the syndrome. Fatty Liver Haemorrhagic Syndrome (FLHS) is brought about by an excessive accumulation of fat in the livers of adult hens which weakens the cellular structure of the liver and allows fatal haemorrhaging to occur. The aetiology of the syndrome is not clear, but a major factor is an excessive intake of dietary energy. However, the involvement of hormonal and toxicological factors, as well as other nutritional factors, is also possible.

Animal Nutritional Physiological Phenomena↗

PubMed1994

Acute fatty liver of pregnancy: an experience in the diagnosis and management of fourteen cases.

OBJECTIVE: Our purpose was to investigate the diagnostic problems and maternal-perinatal outcome in cases of acute fatty liver of pregnancy. STUDY DESIGN: Fourteen cases with acute fatty liver of pregnancy managed during the past 8-years were studied with emphasis on presenting symptoms, admitting diagnosis, laboratory findings, clinical course, maternal complications, and neonatal outcome. RESULTS: The mean gestational age at onset was 34.5 weeks (range 28 to 39). Only seven patients had acute fatty liver of pregnancy as a definite or suspected diagnosis on admission. Computed tomography of the liver was performed on 10 patients, with only two positive results. There were no maternal deaths; however, maternal morbidity was frequent: four patients had hepatic encephalopathy, three pulmonary edema, three ascites, four respiratory arrest, two diabetes insipidus, and 10 had transfusion of blood or blood products to correct either disseminated intravascular coagulation or excessive bleeding. Coagulation abnormalities were common: hypofibrinogenemia (< 300 mg/dl) in 13 patients (93%), prolonged prothrombin time in 12 (86%), and prolonged partial thromboplastin time in 11 (79%). The corrected perinatal mortality was 6.6%. CONCLUSION: Acute fatty liver of pregnancy should be suspected in all patients with symptoms of preeclampsia in the presence of hypoglycemia, low fibrinogen, and prolonged prothrombin time, particularly in the absence of severe abruptio placentae. Computed tomography of the liver has a high false-negative rate in patients with acute fatty liver of pregnancy. In spite of the literature's dismal prognosis, our findings indicate that maternal and perinatal outcomes appear favorable in well-managed patients.

Acute Disease↗

PubMed1987

Acute fatty liver of pregnancy: etiology of fetal distress and fetal wastage.

Acute fatty liver is a rare complication of pregnancy occurring in approximately one in 13,000 deliveries. This disease has been associated with high maternal and fetal mortality rates in the past. Advances in medical care and early recognition and delivery are credited with recent reductions in the maternal and fetal loss seen with this disease. Maternal death is associated with hypoglycemia, hepatic failure, or coagulopathy. The etiology of fetal mortality is not well delineated. Reported is a patient with histologically proved acute fatty liver who developed fetal distress during therapy for coagulopathy. Review of the fetal monitor tracing in conjunction with examination of the placenta have led us to propose that uteroplacental insufficiency may be the cause for fetal distress and fetal wastage in fatty liver of pregnancy.

Acute Disease↗

PubMedDate not supplied

Release of amino acids from fatty livers during organ harvest for transplantation.

Shortage of organ donors presents a perplexing problem in liver transplantation, and improved methods for evaluating the viability of organs prior to implantation are urgently needed. In the present study, the hypothesis was evaluated that grafts from fatty livers release more amino acids than non-fatty controls during organ harvest. Amino acids in graft rinse effluents at the time of harvest and after cold storage were measured by reverse-phase high performance liquid chromatography and compared with plasma aspartate aminotransferase (AST) levels and recipient survival. Twenty-four hours after transplantation of fatty livers, AST levels in recipient rats were increased more than two-fold compared to non-fatty controls (p < 0.01). Survival in the control group was 83 percent, whereas animals receiving fatty livers from ethanol-treated rats survived no longer than 7 days after transplantation (p < 0.05). The rate of release of amino acids from the liver explant was two-fold higher during the harvest procedure (0.5 h) than during the subsequent 23.5 hour cold storage period (435 +/- 70 vs. 186 +/- 14 nmol/ml/hr/g liver, p < 0.001). Further, in the early rinse effluent, amino acids were released about two-fold faster from fatty livers than from controls (p < 0.05). This study demonstrates that the release of amino acids from liver explants increases during the harvesting procedure and is about two-fold higher in fatty livers which fail after transplantation than in surviving controls. It is proposed that amino acid release from explants after organ harvest might serve as a useful marker to evaluate graft function prior to transplantation.

Amino Acids↗

PubMed2000

The spectrum of nonalcoholic fatty liver disease: from steatosis to nonalcoholic steatohepatitis.

Nonalcoholic fatty liver disease (NAFL) has been recognized only in the past 20 years. Autopsy studies indicate it is remarkably common, especially among obese persons and patients with type 2 diabetes. Although fatty liver alone is usually benign, an identifiable subset of patients may be at risk of progression to cirrhosis and liver failure. The role of liver biopsy is controversial. No specific, effective therapy as yet exists, although management of weight, lipid levels, and glucose levels is recommended.

Age Factors↗

PubMed1996

Spontaneous development of fatty liver in ferrets in a toxicology study.

Ferrets were maintained for 12 months on different diets (A, meat and biscuit; B, all meat; C, meat and fish; D, high fibre) to ascertain the cause of spontaneous development of fatty liver. High hepatic triglyceride contents resulted on diets B = C > D; whereas ferrets on diet A (control) showed no accumulation of lipid in liver. Serum triglyceride and total cholesterol were unchanged by diet. These ferrets (F0 generation) were mated with ferrets on the same diet and the offspring (F1 generation), maintained on the same diets as the parents, were killed at 12 months and the livers studied similarly. Histology showed that hepatic lipid accumulation in the F1 generation was identical with that in the same dietary groups of the F0 generation; liver glutathione (GSH) reductase and thiobarbituric acid-reacting substances (an index of lipid peroxidation) were increased in ferrets maintained on diets B, C and D, liver GSH concentration and GSH peroxidase activities were unchanged. Other ferrets fed a high-fat diet (diet A plus 20% w/w beef suet) for 18 days exhibited hepatic lipid accumulation and decreased hepatic cyanide-insensitive palmitoyl CoA oxidation (-30%), but hepatic lauric acid hydroxylation and carnitine acyl transferase activities were unchanged. These data indicate that ferrets on high-fat diets show no increased rates of liver fatty acid oxidation, as seen in rats, but instead accumulate triglyceride in the liver with some degree of lipid peroxidation.

Alkaline Phosphatase↗

PubMed1988

Angiotensin-converting enzyme activity in experimental alcoholic fatty liver of the rat.

Angiotensin-converting enzyme (ACE) activity was found increased in serum of patients with chronic alcoholism. We studied this enzymatic activity in serum and liver tissue of rats with alcoholic fatty liver due to prolonged intake of ethanol with a liquid diet, according to De Carli and Lieber. Serum and liver ACE activity did not show any significant increase in rats with alcoholic fatty liver when compared with controls, whereas gamma-glutamyltransferase activity exhibited a striking enhancement in serum and liver. Our data suggest that ACE is not an alcohol-induced enzyme in the experimental rat model.

Alanine Transaminase↗

PubMed2006

Protection against Western diet-induced obesity and hepatic steatosis in liver fatty acid-binding protein knockout mice.

Liver fatty acid-binding protein (L-Fabp) regulates murine hepatic fatty acid trafficking in response to fasting. In this study, we show that L-Fabp(-/-) mice fed a high-fat Western diet for up to 18 weeks are less obese and accumulate less hepatic triglyceride than C57BL/6J controls. Paradoxically, both control and L-Fabp(-/-) mice manifested comparable glucose intolerance and insulin resistance when fed a Western diet. Protection against obesity in Western diet-fed L-Fabp(-/-) mice was not due to discernable changes in food intake, fat malabsorption, or heat production, although intestinal lipid secretion kinetics were significantly slower in both chow-fed and Western diet-fed L-Fabp(-/-) mice. By contrast, there was a significant increase in the respiratory exchange ratio in L-Fabp(-/-) mice, suggesting a shift in energy substrate use from fat to carbohydrate, findings supported by an approximately threefold increase in serum lactate. Microarray analysis revealed increased expression of genes involved in lipid synthesis (fatty acid synthase, squalene epoxidase, hydroxy-methylglutaryl coenzyme A reductase), while genes involved in glycolysis (glucokinase and glycerol kinase) were decreased in L-Fabp(-/-) mice. Fatty acid synthase expression was also increased in the skeletal muscle of L-Fabp(-/-) mice. In conclusion, L-Fabp may function as a metabolic sensor in regulating lipid homeostasis. We suggest that L-Fabp(-/-) mice are protected against Western diet-induced obesity and hepatic steatosis through a series of adaptations in both hepatic and extrahepatic energy substrate use. (HEPATOLOGY 2006;44:1191-1205.).

Animals↗

PubMed1983

[Acute fatty liver in pregnancy with consumption coagulopathy].

Acute idiopathic fatty liver of pregnancy was observed in a 34-year-old patient. Mother and child survived this complication which has happened in only 10% of the 69 histologically verified cases. On the basis of coagulation studies it may be assumed that consumption coagulopathy had been present initially. This could be pathogenetically relevant in the development of fatty liver of pregnancy.

Acute Disease↗

PubMed2006

Adiponectin and its receptors in rodent models of fatty liver disease and liver cirrhosis.

AIM: To determine circulating and hepatic adiponectin in rodents with fatty liver disease or liver cirrhosis and investigate expression of the adiponectin receptors AdipoR1 on the mRNA and protein level and AdipoR2 on the mRNA level. METHODS: Fat fed rats were used as a model for fatty liver disease and bile duct ligation in mice to investigate cirrhotic liver. Expression of AdipoR1 and AdipoR2 mRNA was determined by real time RT-PCR. AdipoR1 protein was analysed by immunoblot. Adiponectin was measured by ELISA. RESULTS: Systemic adiponectin is reduced in fat-fed rats but is elevated in mice after bile duct ligation (BDL). Hepatic adiponectin protein is lower in steatotic liver but not in the liver of BDL-mice when compared to controls. Adiponectin mRNA was not detected in human liver samples or primary human hepatocytes nor in rat liver but recombinant adiponectin is taken up by isolated hepatocytes in-vitro. AdipoR1 mRNA and AdipoR1 protein levels are similar in the liver tissue of control and fat fed animals whereas AdipoR2 mRNA is induced. AdipoR2 mRNA and AdipoR1 mRNA and protein is suppressed in the liver of BDL-mice. CONCLUSION: Our studies show reduced circulating adiponectin in a rat model of fatty liver disease whereas circulating adiponectin is elevated in a mouse model of cirrhosis and similar findings have been described in humans. Diminished hepatic expression of adiponectin receptors was only found in liver cirrhosis.

Adiponectin↗

PubMed2005

Supplementation with alpha-linolenic acid-rich diacylglycerol suppresses fatty liver formation accompanied by an up-regulation of beta-oxidation in Zucker fatty rats.

Insulin resistance-related obesity and diabetes mellitus are the predominant causes of fatty liver disease. Here we examine the effects of dietary diacylglycerol (DG), which is a minor component of plant oils, on lipid accumulation and the expression of genes involved in lipid metabolism in the liver. The animals were fed diets containing either 10% triacylglycerol (TG), 10% TG + 4% alpha-linolenic acid-rich TG (ALATG) or 10% TG + 4% alpha-linolenic acid-rich diacylglycerol (ALADG) for a period of 1 month. Supplementation with ALADG significantly inhibited hepatic triglyceride accumulation; this was accompanied by the up-regulation of beta-oxidation activity, and acyl-CoA oxidase (ACO) and medium-chain acyl-CoA dehydrogenase (MCAD) mRNA levels. By contrast, no significant changes were observed in the levels of peroxisome proliferator-activated receptor-alpha (PPARalpha) and sterol regulatory element-binding protein-1 (SREBP-1) mRNAs. These results indicate that ALADG might be useful in the prevention of fatty liver formation; this effect could be closely related to the stimulation of lipid catabolism in the liver. In addition, our findings suggest that both acylglycerol structure (that is, the structural difference between TG and DG) and fatty-acid species affect the nutritional behaviour of dietary lipids.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed1993

Acute fatty liver of pregnancy: the hepatologist's view.

Acute fatty liver of pregnancy is a rare clinical entity unique to pregnancy that can lead to hepatic failure and encephalopathy and, if the diagnosis is delayed, to death for the baby and the mother. The characteristic histological picture demonstrates microvesicular fatty infiltration of hepatocytes. Acute fatty liver of pregnancy is a disease of the third trimester of pregnancy. The most significant clinical findings are nausea or vomiting, abdominal pain, jaundice, hepatic encephalopathy, increased transaminase levels, decreased platelet count, increased prothrombin time, and renal failure. Hypertension and proteinuria are common. Liver biopsy is not always necessary for diagnosis but may be useful in atypical cases. The primary therapy is early delivery and supportive care. Both the obstetric team and the medical consultants must have a high index of suspicion for this disease because early delivery is lifesaving and has transformed the prognosis for the mother and the baby. Collaboration between obstetricians and gastroenterologists is necessary to make the diagnosis and also to improve our understanding of this disease of unknown etiology.

Acute Disease↗

PubMed1998

Effect of valine-depleted total parenteral nutrition on fatty liver development in tumor-bearing rats.

Valine-depleted amino acid imbalance, while having a suppressive effect on tumor growth, may induce fatty liver. We administered valine-depleted total parenteral nutrition (TPN) solution to rats subcutaneously transplanted with ascites containing hepatoma AH-109A and examined the time course of the development of fatty liver. An accumulation of fatty vacuoles was observed in hepatocytes on day 4. To prevent the development of fatty liver in tumor-bearing rats, we administered a small amount of valine in addition to the valine-depleted imbalance solution via the central vein. Such treatment, however, resulted in neither the prevention of fatty liver development nor the suppression of tumor growth. To supply valine to the liver, we administered a low concentration of valine via the portal vein simultaneously with central venous administration of valine-depleted TPN solution. As a result, the peripheral blood valine level of these rats was < 0.5 that of the control group, but the valine in the liver was maintained at the same level as that of the control group, and accumulation of triacylglycerols in the liver was slight. However, the suppressive effect on tumor growth was maintained, as the tumor weight was suppressed to almost the same degree as that of rats administered only the valine-depleted solution.

Amino Acids↗

PubMed2003

Diagnosis of fatty liver disease: is biopsy necessary?

Non-alcoholic fatty liver disease is increasingly being recognized as an important and common condition, affecting approximately 20% of the general population. Although liver biopsy is currently the gold standard for diagnosis, there is a need for less invasive methods. Imaging by ultrasound, computerized tomography and magnetic resonance are all able to demonstrate fat. In this paper, these three imaging techniques are critically assessed. Ultrasound, although probably not the most reliable imaging method, has many advantages and, when positive, gives a high degree of certainty of the diagnosis depending on the prevalence of fatty liver in the population being studied. Unlike liver biopsy, none of these techniques is able to differentiate simple steatosis from non-alcoholic steatohepatitis.

Biopsy↗

PubMed1981

Effect of diisopropyl 1,3-dithiol-2-ylidenemalonate (NKK-105) on fatty liver induced by carbon tetrachloride.

The therapeutic effect of diisopropyl 1,3-dithiol-2-ylidenemalonate (NKK-105) on the fatty liver induced by carbon tetrachloride (CCl4) was studied. The recovery from elevated liver triglyceride levels induced by CCl4 required over 20 days in 35 week-old rats, but 14 days in 6 week-old rats. This indicates that 35 week-old rats are useful for studying the therapeutic effect of NKK-105 on fatty liver. In rats with CCl4-induced fatty liver, NKK-105 lowered the hepatic triglyceride level, accelerated the rate of triglyceride release from the liver, enhanced the incorporation of 14C-leucine into microsomal protein, and increased the RNA content in microsomes. These data suggest that NKK-105 exerts a curative effect on CCl4-induced fatty liver by improving the impaired protein synthesis and by promoting lipoprotein secretion.

Animals↗

PubMed2001

Increased generation of reactive oxygen species in isolated rat fatty liver during postischemic reoxygenation.

BACKGROUND: Whether fatty infiltration of the liver influences the generation of reactive oxygen species (ROS) during reperfusion is unclear. Thus, this study aimed to compare the ROS formation that occurs during postanoxic reoxygenation in isolated normal and fatty livers. METHODS: Isolated livers from fed Sprague-Dawley rats with normal or fatty livers induced by a choline-deficient diet were reperfused at 37 degrees C for 60 min with an oxygenated medium containing 10 microM of lucigenin after 1 hr of warm ischemia. Superoxide anion generation was assessed by the chemiluminescence (CLS) signal emitted from the organ surface. The hepatic content of malondialdehyde (MDA) and glutathione was determined at the end of reperfusion. Tissue injury was evaluated by the liver histology and the alanine aminotransferase (ALT) release in the perfusate. RESULTS: CLS started rapidly with reoxygenation and it diffused to the whole organ in both groups. However, CLS emission was significantly higher in fatty liver (after 10 min: 812.425+/-39.898 vs. 294.525+/-21.068 photons/cm2/sec; P<0.01). A greater concentration of MDA was measured at the end of reoxygenation in fatty liver. Finally, the liver histology and the ALT release indicated a greater injury in steatotic than normal liver. CONCLUSIONS: The CLS technique allows a direct visualization and comparison of ROS generation from the organ surface. Fatty infiltration increases ROS generation in the liver during postischemic reoxygenation, likely leading to the greater lipid peroxidation observed in these experiments. The increased oxidative stress may contribute to the reduced tolerance of steatotic livers to ischemia-reperfusion injury.

Alanine Transaminase↗