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PubMed1986

[Acute fatty liver of pregnancy].

A case is reported of acute fatty liver of pregnancy with maternal and foetal survival inspite of jaundice, encephalopathy, renal failure, gastro-intestinal haemorrhage and serious coagulation problems. The acute fatty liver is a rare disease of unknown aetiology which occurs during the third trimester of pregnancy. Early diagnosis based on liver biopsy obtained by the transjugular route, immediate delivery of the foetus and intensive care improve an otherwise fatal prognosis.

Adult↗
PubMed1994

Acute fatty liver of pregnancy and long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency.

The pathogenesis of acute fatty liver of pregnancy is unknown, but similarities in the clinical presentation and the histological appearance of the liver with those found in children with metabolic defects in the intramitochondrial beta-oxidation pathway of the liver suggest that a disturbance in hepatic fatty acid oxidation may play a role. We report a woman with acute fatty liver of pregnancy who gave birth to a seemingly normal full-term infant who was seen at 4 mo of age with hypoglycemia, coma and profound hepatic steatosis. The infant had a defect in fatty acid oxidation, long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency, and the mother proved to be heterozygous for this metabolic condition. We hypothesize that the interaction of an affected fetus with a female heterozygous for this defect in fatty acid oxidation in the late third trimester accounts for some cases of acute fatty liver of pregnancy.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1999

Total serum bile acid concentrations in dairy cows with fatty liver and liver failure.

In forty-five Holstein Frisian dairy cows (1-6 weeks post partum; mean age: 5.1 +/- 1.2 years) the serum total bile acid concentrations (SBA) were measured enzymatically. In all cows a left sided abomasal displacement was corrected surgically by right side laparotomy and omentopexy three days before investigation. The liver fat content was determined in all cows histologically. Liver failure was assumed if typical clinical signs (ataxia, general depression, recumbency or coma), an increased venous plasma ammonia level (> 35 mumol/l) and a decreased plasma amino acid index (< 4.0) were found. Cows without liver failure (N = 29) were grouped according to the liver fat content as cows with mild (N = 5), moderate (N = 19) or severe hepatosteatosis (N = 5). Histological examination of liver biopsies in cows with liver failure (N = 16) revealed in twelve cases a severe fatty liver and in four cases a hydropic degeneration of the liver tissue. Although in cows without liver failure mean SBA concentrations were higher in the group with moderate (47.3 +/- 30.9 mumol/l) or severe fatty liver (32.9 +/- 21.7 mumol/l) than in that with mild lipidosis (18.0 (16.8 mumol/l), differences were not significant. The mean SBA concentration in cows with liver failure (70.5 +/- 49.5 mumol/l) was only significantly (p < 0.05) increased compared to cows with uncomplicated mild hepatic lipidosis. In conclusion, the determination of SBA concentrations is of little value in the recognition of fatty liver or even liver failure due to the considerable variance of SBA concentrations in dairy cows.

Abomasum↗
PubMed2006

Melatonin ameliorates nonalcoholic fatty liver induced by high-fat diet in rats.

Nonalcoholic fatty liver disease (NAFLD) is an increasingly recognized condition that may progress to end-stage liver disease, which ranges from simple steatosis to steatohepatitis, advanced fibrosis, and cirrhosis. Oxidative stress and lipid peroxidation are key pathophysiological mechanisms in NAFLD. We investigate the preventive effects of intraperitoneal administration of melatonin (2.5, 5, 10 mg/kg, daily, respectively) in NAFLD rats induced by high-fat diets for 12 wk. Liver damage was evaluated by serological analysis, serum and hepatic lipid assay as well as hematoxylin-eosin staining in liver sections. Oxidative stress and lipid peroxidation were assessed by measuring malondialdehyde (MDA) levels and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in liver. The results showed that high-fat diet induced oxidative stress with extensive liver steatosis in rats. Melatonin (5 or 10 mg/kg) was effective in reducing hepatic steatosis and inflammation with lowering serum alanine aminotransferase, aspartate aminotransferase, and levels liver total cholesterol and triglycerides in high-fat diet rats. Moreover, melatonin (2.5, 5, 10 mg/kg) increased SOD and GSH-Px activities and the 10 mg/kg dose of melatonin reduced MDA levels in liver. This study shows that melatonin exerts protective effects against fatty liver in rats induced by high-fat diet possibly through its antioxidant actions.

Animals↗
PubMed1988

[Acute fatty liver of pregnancy. Diagnostic value of hyperuricemia in the pre-jaundice stage].

Acute fatty liver of pregnancy, with a case history where an early diagnosis could have been made, and a review of the French literature. Acute fatty liver of pregnancy, or Sheehan's syndrome is a rare but very serious complication of pregnancy. The disease is demonstrated by vomiting, abdominal pain and a high level of uric acid in the blood before jaundice is noted. Within a few days the triad of jaundice, pruritus and encephalopathy occur. These are often associated with toxaemia of pregnancy and with polyuria and polydipsia. A raised white blood count and a high level of bilirubinemia are almost always present. The outlook is very serious when haemorrhage appears. This malignant form of the disease is characterised by liver and kidney failure. Liver biopsy confirms the diagnosis. The prognosis is related to an early diagnosis and is good when labour is induced or caesarean section performed. Acute fatty liver of pregnancy is an emergency from the diagnostic as well as the therapeutic angles.

Acute Disease↗
PubMed2004

Animal models of nonalcoholic fatty liver disease and steatohepatitis.

As occurs in people, nonalcoholic fatty liver disease (NAFLD) is associated strongly with obesity, diabetes, and dyslipidemia in experimental animals. There are many animal models that have been used to investigate the pathogenesis of nonalcoholic fatty liver disease. Most of this work has used mice or rats that are fed diets high in fat or carbohydrates, or mice that exhibit a genetic deficiency of a satiety factor such as leptin, 5-adenosylmethionine,or enzyme deficiencies in fatty acid oxidation. The purpose of this article is to update information regarding animal models in the pathogenesis of NAFLD.

Animals↗
PubMed1996

Mechanism of insulin resistance and hyper-insulinemia in fatty liver.

Hyperinsulinemia and insulin resistance are common features seen in most liver diseases. The present study was carried out on an experimental model of fatty liver (tetracycline induced) in albino rats. Significantly elevated levels of both peripheral plasma insulin and plasma glucose concentrations were recorded in both the fasting state and after an oral glucose intake in the tetracycline-treated rats. The presence of hyperinsulinemia accompanying hyperglycemia is considered a sign of insulin resistance. Peripheral insulin resistance has been proved in this work by the reduced "A" value which refer to the peripheral insulin activity (sensitivity) in fatty liver rats compared to normal rats. The hyperinsulinemia recorded here was due to pancreatic hypersecretion and not a result of reduced hepatic degradation. Hypersecretion of insulin was clearly determined by measuring the level of immunoreactive insulin (IRI) in pancreatic vein which exhibited a significant rise in tetracycline-treated rats, and there was a positive correlation between the pancreatic venous and peripheral venous insulin in the basal state and after 30 min. of oral glucose administration. Hepatic degradation of insulin was not a cause as evidenced by First: the amount of insulin secreted and insulin consumed were significantly higher in fatty liver rats than normal controls. Second: the whole body extraction ratio or insulin degradation was not significantly different in the tetracycline-treated rats from the normal rats. The present data suggests that insulin resistance and hyperinsulinemia underlie the observed metabolic disturbances that characterize fatty liver disease.

Animals↗
PubMed1981

[Patients with fatty liver. Study of ten years course of the disease (author's transl)].

Patients with fatty liver of grades I and II were re-examined by liver biopsy after a 10 years' interval. Only two patients showed improvement in the original findings. In each case up to about half of the material for investigation showed an unchanged stage of fatty liver or a deterioration. In the group with an unchanged clinical picture of grade II fatty infiltration and in the cases with a tendency to deteriorate, an accumulation of etiological factors was noted. Extensive histories proved that the patients had not altered their living habits in the past 10 years. This means that the prognosis of fatty liver with regard to regression of an originally established stage is very unfavorable, because the patients' understanding seems not to be very great.

Biopsy↗
PubMed1991

Induction of fatty liver by fasting in suncus.

We found that a fatty liver was easily induced in a novel experimental animal, Suncus murinus (suncus), by withholding food. Hepatic triglyceride content increased linearly for up to 24 h after fasting in these animals. Serum levels of neutral lipids are very low in the fed state compared with those in rats, and decreased significantly after 24 h fasting. On the other hand, serum free fatty acids, which are at the same level in fed animals as in rats, increased threefold in the fasting suncus. In order to learn whether the fatty liver induced by fasting is an unusual physiological state or a pathological on-going state in suncus, they were refed after 24 h fasting. Refeeding resulted in a decrease in hepatic triglyceride content to the level of fed animals. Serum lipid levels, which decreased with fasting, returned to those of fed animals. This evidence indicates that hepatic lipid secretion is impaired even in a physiological state to some extent and that starvation causes increasing influx of free fatty acid to the liver, which might be followed by esterification and result in triglyceride accumulation in the liver. In conclusion, hepatic lipid and lipoprotein metabolism is unique to the suncus, which is a useful animal model for the study of intra-hepatic lipid transport.

Animals↗
PubMed2000

Metformin reverses fatty liver disease in obese, leptin-deficient mice.

There is no known treatment for fatty liver, a ubiquitous cause of chronic liver disease. However, because it is associated with hyperinsulinemia and insulin-resistance, insulin-sensitizing agents might be beneficial. To evaluate this possibility, insulin-resistant ob/ob mice with fatty livers were treated with metformin, an agent that improves hepatic insulin-resistance. Metformin improved fatty liver disease, reversing hepatomegaly, steatosis and aminotransferase abnormalities. The therapeutic mechanism likely involves inhibited hepatic expression of tumor necrosis factor (TNF) alpha and TNF-inducible factors that promote hepatic lipid accumulation and ATP depletion. These findings suggest a mechanism of action for metformin and identify novel therapeutic targets in insulin-resistant states.

Adenosine Triphosphate↗
PubMed2005

[Clinical study on treatment of fatty liver by shennong ganzhining].

OBJECTIVE: To observe the therapeutic effect and safety of Shennong Ganzhining (SG) in treating fatty liver. METHODS: One hundred and ninety patients with fatty liver were randomly divided into two groups. The 142 patients in the treated group received SG and the 48 in the control group received Zhibituo treatment for 3 months. The comprehensive therapeutic effect after treatment, symptoms, signs, liver function, blood lipids and blood viscosity, as well as iconographic parameters were observed. RESULTS: The total effective rate in the treated group was 80.98%, which was higher than that in the control group (75.00%), showing significant difference statistically (P < 0.05). Satisfactory effect was obtained in recovery of liver function, improvement of blood lipids, blood viscosity and iconographic parameters, no severe adverse reaction occurred. CONCLUSION: SG is obviously effective in treating fatty liver with favorable safety.

Adolescent↗
PubMed2003

Effects of radiation on fatty liver and metabolic coronary risk factors among atomic bomb survivors in Nagasaki.

In order to clarify the basic mechanism(s) linking radiation exposure and coronary heart disease (CHD), we here collected ultrasonographic data on fatty liver and measured levels of metabolic CHD risk factors from November 1990 through October 1992 in 1,517 Nagasaki atomic bomb survivors (575 men and 942 women). Using a cross-sectional study design, we examined the effects of radiation dose on fatty liver and CHD risk factors by means of a multiple logistic regression model. Fatty liver was related to the metabolic CHD risk factors associated with insulin resistance syndrome: obesity, hypertension, hypercholesterolemia, low high density lipoprotein (HDL)-cholesterol, hypertriglyceridemia, and abnormal glucose metabolism. Radiation dose was positively related to fatty liver, low HDL-cholesterol, and hypertriglyceridemia, whereas it had no effects on obesity, hypertension, hypercholesterolemia, or abnormal glucose metabolism. The present results suggested that radiation dose was related to 1) fatty liver, which clustered the metabolic CHD risk factors associated with insulin resistance syndrome and 2) atherogenic lipid profiles. It is suggested that these associations are involved in the basic mechanism(s) linking radiation exposure and CHD.

Aged↗
PubMed1983

Extent of retention of 2-monoglyceride backbone of diet fat in alcohol-induced fatty liver.

This study was carried out to determine whether hepatic triglyceride (TG) synthesis is a major determinant in the development of fatty liver induced by chronic ethanol ingestion. For this purpose, the degree to which the 2-monoglyceride (MG) backbone of dietary fat was retained in the accumulated TG of fatty liver was examined. Triglycerides were isolated from diet and from the liver and plasma of rats maintained for four weeks on a Lieber-DeCarli liquid ethanol diet. Pancreatic lipase hydrolysis of the TG from these three sources was carried out and the MG produced was analyzed for the fatty acid composition. Almost all of TG in fatty liver and that released to plasma retained the MG structure which originated from diet fat. This result demonstrates that the de novo glyceride synthesis or transacylation reactions do not have a major role in the production of TG in alcohol-induced fatty liver.

Animals↗
PubMedDate not supplied

Aortic atherosclerosis in nonlaying hens with fatty liver syndrome.

Ten laying hens with low plasma cholesterol levels and no signs of fatty liver syndrome were examined at necropsy. Liver coloration and deposition of body fat were not abnormal in such hens. Eleven nonlaying hens had signs of fatty liver syndrome. They were out of production for 1 to 3 months and had elevate plasma cholesterol levels. At necropsy, such hens had yellow livers, heavy deposits of body fat, and several involuted egg yolks, which were dark yellow. Intimal plaques were observed by light microscopy in the abdominal aortas of hens with low plasma cholesterol levels; the plaques contained little or no lipid and were composed of three or four rows of modified smooth-muscle cells. Aortic intimal plaques of hens with high plasma cholesterol levels were composed of 16 to 18 rows of modified smooth-muscle cells when examined by light microscopy. The plaques contained intracellular and extracellular lipid, indicating aortic atherosclerosis. Electron-microscopic observations of the abdominal aortas of both groups of hens were similar to light-microscopic observations, except that lipid, including cholesterol clefts, was seen both intracellularly and extracellularly in the thickened tunica intima of hens with high plasma cholesterol values. Thus, the presence of aortic atherosclerosis was confirmed by electron microscopy. It is suggested that the endogenous hypercholesterolemia and cessation of egg production, characteristic of severe fatty liver syndrome, originated from the reabsorption of involuted egg yolks and that such reabsorption caused the development of aortic atherosclerosis and deposition of excess body fat.

Animals↗
PubMed1984

[Experimental study on quantitative evaluation of fatty liver by computed tomography].

Biochemical, histological and CT examinations of the liver were performed in 32 rabbits on significance of measuring CT values in the diagnosis of fatty liver. In 2 groups of rabbits, in which 2g/kg/day and 4g/kg/day of fat emulsion were administered intravenously for 4 weeks respectively, post-treatment reduction in CT value of light degree was observed. In a group, in which 8g/kg/day were given, there was a sufficient reduction in CT value for giving diagnosis of fatty liver of moderate degree. Significant correlation was found between changes in CT value of the liver on the one hand and contents of triglyceride, total cholesterol and cholesterol ester in the liver on the other hand, while there was, no significant correlation between changes in CT value and contents of phospholipid, protein and water. Significant correlation was found between changes in CT value of the liver and degrees of histological fat accumulation in the liver cells. It has been evidenced experimentally that prolonged administration of fat emulsion may cause fatty liver, and that measurement of CT values of the liver is a non-aggressive method of diagnosing fatty liver.

Animals↗
PubMed1979

Accentuation of white phosphorus induced fatty liver by phenobarbitone in male rats compared to female rats.

The possible influence of a potent enzyme inducer, phenobarbitone, on white phosphorus fatty liver, was studied. Pretreatment by phenobarbitone for four days in white phosphorus poisoned rats provoked a decrease in mortality and an increase in hepatic triglycerides (fatty liver) in male rats. The activity of uridine diphosphoglucuronyl transferase (UDPGT), an inducible enzyme, is not modified by this pretreatment in white phosphorus poisoned rats. The accentuation of white phosphorus fatty liver by phenobarbitone in male rats could be explained by an increased hydroxylation of testosterone, thus counteracting the protective effect of this hormone on fatty liver.

Animals↗
PubMed1996

Radiologic studies in acute fatty liver of pregnancy. A review of the literature and 19 new cases.

OBJECTIVE: Radiologic findings thought to be characteristic of acute fatty liver of pregnancy have been described in a limited number of cases. We describe wide experience with liver imaging of this disease. STUDY DESIGN: A retrospective review was performed on charts from 1982 to 1994 to identify those patients with acute fatty liver of pregnancy who had radiologic studies. RESULTS: Twenty-eight patients with acute fatty liver of pregnancy were identified, for an incidence of 1/6,692 births. Nineteen patients underwent at least one imaging study, and seven had more than one. Findings consistent with fatty infiltration of the liver are found in 3/11 patients with ultrasound, 5/10 with computed tomography (CT) and 0/5 with magnetic resonance imaging (MRI). Three patients with normal ultrasound scans subsequently had evidence of fatty filtration on CT scan. CONCLUSION: Detection of fat in the liver of patients with acute fatty liver of pregnancy with current imaging techniques is limited and did not contribute to the management of patients in this series. Further studies are necessary to define to role of MRI--in particular, spectroscopy.

Adult↗