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PubMed1982

Dietary and plasma phosphorus in hens with fatty liver syndrome.

Plasma inorganic phosphorus was determined in two experiments in hens that had fatty liver syndrome. In Experiment 1, plasma inorganic phosphorus was determined in twelve strains of hens all fed the same diet. Plasma inorganic phosphorus immediately following oviposition was elevated in all strains. The two strains in the first experiment with the highest as well as the two strains with the lowest plasma inorganic phosphorus were used in the second experiment. Each of the four strains were subdivided into three groups of 60 hens each and fed a practical layer diet containing either .30, .75, or 1.40% total phosphorus and 3.4% calcium. Significant differences were found in plasma inorganic phosphorus between strains fed the three dietary phosphorus levels. Results indicated that plasma inorganic phosphorus is related to dietary phosphorus in hens with an elevated plasma inorganic phosphorus level associated with fatty liver syndrome.

Animals↗
PubMed2005

Absence of fatty liver in familial hypobetalipoproteinemia linked to chromosome 3p21.

Our aim was to ascertain whether fatty liver may be present in the genetic form of familial hypobetalipoproteinemia (FHBL) linked to a susceptibility locus on chromosome 3p21. Three genetic forms of FHBL exist: (a) FHBL caused by truncation-specifying mutations of apolipoprotein B (apoB), (b) FHBL linked to chr3p21, and (c) FHBL not linked either to APOB or to chr3p21. Fatty liver is common in apoB-defective FHBL. Hepatic fat contents were quantified by magnetic resonance spectroscopy in 16 subjects with 3p21-linked FHBL, 32 subjects with apoB-defective FHBL, and 39 sex- and age-matched controls. Mean liver fat of 3p21 subjects was similar to controls and approximately 60% lower than apoB-defective FHBL subjects ( P = .0012). Indices of adiposity (body mass index, waist/hip ratio) and masses of abdominal subcutaneous, retroperitoneal, and intraperitoneal adipose tissue (IPAT) were quantified by MR imaging. Mean measures of adiposity were similar in the 3 groups, suggesting that adiposity per se was not responsible for differences in liver fat. Liver fat content was positively correlated with IPAT. The intercepts of regression lines of IPAT on liver fat content were similar in controls and 3p21, but higher in apoB-defective FHBL subjects. The slopes of the lines were steepest in apoB-defective, intermediate in 3p21, and flattest in controls. Lipoprotein profiles and very low density lipoprotein-apoB100 kinetics of 3p21 and apoB-defective groups also differed. Thus, 2 genetic subtypes of FHBL also differ in several phenotypic features.

Adipose Tissue↗
PubMed1982

Role of glucose on fatty liver formation in pyridoxine-deficient rats.

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.

Animals↗
PubMed2000

[Experimental study on inhibitory effect of Chinese herbal compound on hepatocyte cytochrome P450 II E1 expression in rat model of nonalcoholic fatty liver].

OBJECTIVE: To study the effect of Chinese herbal compound (CHC) on hepatocyte cytochrome P450 II E1 expression in rat model of nonalcoholic fatty liver (NFL). METHODS: CHC was given to the models of NFL formed by high fat diet, and changes on pathology of liver and hepatocyte cytochrome P450 II E1 expression, as well as the contents of malonyldialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), vitamin E (VitE) and triglyceride (TG) in liver were observed and compared with those in the control group. RESULTS: The fatty degeneration of liver recovered to normal basically in the CHC group. Immunohistochemical examination showed that CHC could inhibit the hepatocyte cytochrome P450 II E1 expression markedly, and restore the liver contents of MDA, SOD, GSH, VitE and TG to near normal range. CONCLUSION: CHC could inhibit the hepatocyte cytochrome P450 II E1 expression markedly in rats with fatty liver, therefore, has the effect of preventing fatty liver.

Animals↗
PubMed2004

Evaluating the efficacy and safety of Danning Pian in the short-term treatment of patients with non-alcoholic fatty liver disease: a multicenter clinical trial.

BACKGROUND: Currently, the management of non-alcoholic fatty liver disease (NAFLD) is less than certain. Some choleretic might be of potential benefit and deserve further evaluation. This multicenter clinical trial was designed to evaluate the efficacy and safety of Chinese herbal medicine Danning Pian (composed of rhubarb, grant knotweed, dried green orange peel and dried old orange peel) in the short-term treatment of patients with NAFLD. METHODS: The efficacy and safety of Danning Pian in the short-term treatment of NAFLD were investigated in 232 patients by a multicenter clinical trial during the period of July 1999 to February 2000. The patients consisting of 189 males and 43 females with an average age of 46.1+/-8.7 years were given 3-5 tablets of Danning Pian orally thrice daily for 3 months in addition to the other comprehensive therapy. The effects of Danning Pian on NAFLD were evaluated by the improvement of clinical symptoms, blood lipids, hepatic enzymes and liver ultrasonographic features. The drug safety was monitored by physical examinations, vital signs, and laboratory tests in addition to the assessment of the adverse events. RESULTS: All the enrolled patients completed the study except one whose serum ALT level was moderately increased during the therapy with Danning Pian. The effective rate of Danning Pian for the improvement of clinical symptoms, serum ALT levels, blood lipid and fatty liver was 85.8%, 78.2%, 39.6% and 34.0% respectively after the therapy for 3 months. However, the reduction of excessive body weight and waistline did not reach the significant level on the whole after the therapy. The general mild adverse events included diarrhea, skin rash and mild to moderate elevation of serum ALT level. The incidence of adverse reaction was 15.1%. CONCLUSION: The data of this trial indicate that Danning Pian is effective and safe, generally well-tolerated without severe adverse events, in the treatment of patients with NAFLD over a 3-month period.

Adult↗
PubMed1975

Metabolic studies on the development of ethanol-induced fatty liver in KK-Ay mice.

Mechanisms involved in the development of the alcoholic fatty liver in KK-Ay mice were investigated. Incorporation studies using [14C]acetate and [3H]palmitate indicated that the half-life of hepatic triglycerides was doubled in the ethanol-ingesting mice, and utilization of the exogenous fat was significantly increases as compared with that of the control. No persistent alteration was recognized in hepatic oxidation of palmitate, as estimated by in vitro experiments using liver slices obtained from control and ethanol-drinking mice. Enzymic studies indicated that the activities of acetyl COA carboxylase, ATP citrate lyase, malic enzyme, and 6-phosphogluconate dehydrogenase were increased with ethanol drinking. The increment in hepatic triglycerides accumulated during ethanol ingestion was largely accounted for by palmitoleic, oleic, and linoleic acids. These findings demonstrated an augmentation in hepatic lipogenesis as well as an increased utilization of exogenous fats. Ethanol drinking did not cause any appreciable change in plasma triglyceride level and metabolism of adipose tissue. In summary of the present studies, accelerated lipogenesis and increased utilization of the dietary fats may be possible causal factors in the alcoholic fatty liver of KK-Ay mice.

ATP Citrate (pro-S)-Lyase↗
PubMed2005

Clinicopathological significance of oxidative cellular damage in non-alcoholic fatty liver diseases.

Oxidative stress may play an important role in the progression of simple steatosis to non-alcoholic steatohepatitis (NASH). Oxidative stress is generated through multiple sources, including oxidation of free fatty acids, cytochrome P4502E1, iron overload, and necro-inflammatory cytokines including tumor necrosis factor-alpha. Oxidative stress may trigger damage to cellular membranes and nuclear DNA, which results in lipid peroxidation and oxidative DNA damage, respectively. Here, we present our data on intrahepatic localization and clinico-pathological significance of oxidative stress-induced cellular damage in the patients with non-alcoholic fatty liver diseases (NAFLD). Our subjects were 23 patients with non-alcoholic simple fatty liver, 17 with NASH, and 7 with normal liver (control). Hepatic expression of 4-hydroxy-2'-nonenal (HNE) and 8-hydroxydeoxyguanosine (8-OHdG), as reliable markers of lipid peroxidation and oxidative DNA damage, was in situ detected by using commercially available monoclonal antibodies. While no HNE adducts were observed in control livers, they were frequently detected in NAFLD. In NASH, the localization of the HNE adducts was in the cytoplasm of sinusoidal cells and hepatocytes with a predominance in zone 3. The grade of necro-inflammation as well as the stage of fibrosis significantly correlated with the HNE labeling index. With respect to 8-OHdG, although no 8-OHdG expression was observed in normal liver and only a few in non-alcoholic simple fatty liver, 11 of 17 patients with NASH (65%) exhibited nuclear expression of 8-OHdG in hepatocytes and sinusoidal cells in areas of active inflammation. The 8-OHdG index significantly correlated with the grade of necro-inflammation, but not with the stage of fibrosis. Our observations suggest that oxidative cellular damage occurs frequently in livers with NAFLD and may be associated with some clinico-pathological features of NAFLD including liver fibrosis and possibly, hepatocarcinogenesis.

Journal Article↗
PubMed2004

Non-alcoholic fatty liver disease: a multicentre clinical study by the Italian Association for the Study of the Liver.

AIM: To define the characteristics of the Italian patient presenting non-alcoholic fatty liver disease. PATIENTS AND METHODS: A total of 305 patients with abnormally high plasma aminotransferase and/or gamma-glutamyl-transpeptidase levels for at least 12 months, with no known cause of chronic liver damage, were consecutively enrolled in the study. Clinical, routine biochemical and liver histology investigations were carried out in all patients. Also evaluated were: (a) oral glucose load; (b) insulinaemia and insulin-resistance using the HOMA test model; and (c) plasma endotoxaemia, total antioxidant plasma capability, tumour necrosis factor-alpha, plasma interleukin-6 and -10 levels. Malondialdehyde and 4-hydroxynonenal content were determined on liver samples from 120 patients. RESULTS: The majority of patients were young overweight or obese males, with dyslipidaemia (20-60%), diabetes (10.5%), hyperinsulinaemia (40%), hyperferritinaemia (35%). Endotoxaemia was negative in all patients and cytokines were only sporadically altered. Total antioxidant plasma capability was decreased in 38.4% of the patients. Eighty percent of the cases had histological steatosis with a mild degree of inflammation and fibrosis. Seven patients had cirrhosis. Lipid peroxidation markers were increased in 90% of the cases, inversely correlated with fibrosis. Even if at univariate analysis, age, ferritin and tissue 4-hydroxynonenal were independent factors of steatosis (P < 0.01), and insulin, HOMA and ferritin of inflammation and fibrosis (P < 0.01), at multivariate analysis no single factor was found to be an independent predictor of hepatic lesions. CONCLUSIONS: The typical Italian patient with non-alcoholic fatty liver disease is a young male, obese, not diabetic, with a variable incidence of dyslipidaemia and hyperinsulinaemia. Only liver biopsy may define the type of liver damage.

Adolescent↗