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PubMed2000

Warm ischemia and reperfusion injury in diet-induced canine fatty livers.

BACKGROUND: Fatty liver is associated with primary nonfunction after liver transplantation, contributing a shortage of suitable liver grafts. Because extensive investigation of mechanisms underlying such nonfunction has been limited largely to rodents, we made a new fatty liver model in dogs and studied primary nonfunction after warm ischemia. METHODS: We developed a diet rich in fat but deficient in choline to induce fatty change in canine liver and investigated effects of 60 min of warm ischemia and reperfusion in dogs with such fatty livers. RESULTS: Microscopically evident steatosis increased with duration of dietary manipulation (up to 12 weeks), as did hepatic total lipid and triglyceride levels. No dog with >30% of steatotic hepatocytes, >445 mg/g hepatic total lipid or >145 mg/g hepatic triglyceride survived after 60 min of warm ischemia. Arterial ketone body ratios decreased and blood endotoxin increased after reperfusion in nonsurvivors. The main histologic finding in livers of nonsurvivors was marked sinusoidal congestion. CONCLUSIONS: Damage to hepatocytes and nonparenchymal cells after warm ischemia and reperfusion was thought to be closely related to sinusoidal microcirculatory disturbances in fatty livers. The canine fatty liver model reported here may be useful in studying the pathology of primary nonfunction and in establishing criteria for allowable degrees of fatty change in potential liver grafts.

Alanine Transaminase↗
PubMedDate not supplied

Association of nonalcoholic fatty liver disease with insulin resistance: is OGTT indicated in nonalcoholic fatty liver disease?

Nonalcoholic fatty liver disease (NAFLD) is frequently associated with type 2 diabetes mellitus, obesity, and dyslipidemia. We tested the hypothesis that there may be an association between NAFLD and insulin resistance (IR); and its correlation with glucose tolerance status of subjects who aren't known patients with diabetes. One hundred and seventy-six consecutive patients with elevated serum aminotransferase levels and bright liver were evaluated. Sixty-two patients were excluded from the study. Age, gender, height, weight, body mass index, waist circumferences, and family history of diabetes were recorded. Fasting plasma glucose, insulin, lipid profile were measured. A standard oral glucose tolerance test (OGTT) was performed and the index of IR was calculated according to the HOMA method. Patients with a normal glucose tolerance formed group 1 (64 patients) and patients with impaired or diabetic glucose tolerance group 2 (50 patients). Age, female sex, family history of type 2 diabetes, fasting insulin, fasting plasma glucose and HOMA-R index were statistically significantly different between the groups. Although the subjects in the study are not known patients with diabetes, the prevalence of impaired or diabetic glucose tolerance was prominent. In conclusion, performing OGTT in cases with nonalcoholic fatty liver disease may be useful for early screening of diabetes mellitus.

Adult↗
PubMed2006

Distinguishing nonalcoholic steatohepatitis from fatty liver: serum-free fatty acids, insulin resistance, and serum lipoproteins.

OBJECTIVES: The prognosis of nonalcoholic fatty liver disease is determined by liver biopsy; steatohepatitis can be progressive whereas fatty liver is benign. Insulin resistance and increased hepatic-free fatty acids are central to the pathophysiology of this disorder. Our objective was to assess whether serum-free fatty acids, lipoproteins, and insulin resistance are increased in steatohepatitis compared with fatty liver and healthy controls, and thus may be potential noninvasive markers for liver disease severity. METHODS: Fifteen subjects with biopsy proven nonalcoholic steatohepatitis, 15 with histological fatty liver, and 15 healthy controls were enrolled. Fasting serum glucose and insulin levels, serum-free fatty acids, HDL, LDL, and cholesterol were collected from each subject. Insulin resistance was calculated using the homeostasis assessment model. RESULTS: Insulin resistance, LDL, and cholesterol-to-HDL ratio values were significantly higher in steatohepatitis, whereas HDL was significantly lower compared with both fatty liver and controls. Free fatty acids were similar in all groups. CONCLUSIONS: Along with insulin resistance, serum LDL, and cholesterol-to-HDL ratio values increase with worsening severity of liver histology, and serum HDL values decline. Free fatty acids, however, do not vary between groups.

Adult↗
PubMed2003

Spontaneous development of hepatocellular carcinomas in the FLS mice with hereditary fatty liver.

The fatty liver Shionogi (FLS) mouse is an inbred strain that develops spontaneous fatty liver (hepatic steatosis) chronically without obesity. Here, we reported that the mice develop spontaneous hepatocellular tumors with high incidences. The mice with age of over 1 year frequently developed whitish protuberant nodules in the livers, which were histologically diagnosed as hepatocellular adenoma and/or carcinoma (HCC). An incidence of HCC was 12/30 (40%) in males at 15-16 months of age, while in females that was 0/36 at 13-16 months and 4/42 (9.5%) at 20-24 months. Furthermore, histological examinations showed that after 2-4 months of age mononuclear cell infiltration and clusters of foamy cells appear in the fatty liver with elevated serum alanine aminotransferase, suggesting presence of inflammatory responses and liver injury. These observations show that the FLS mice develop hepatocellular tumors following steatohepatitis. The mouse might be a good animal model for investigating liver tumor and non-alcoholic steatohepatitis.

Age Factors↗
PubMed2003

Effect of hens fed dietary flaxseed with and without a fatty liver supplement on hepatic, plasma and production characteristics relevant to fatty liver haemorrhagic syndrome in laying hens.

1. Two long-term experiments were conducted with Single Comb White Leghorn (SCWL) hens (line UCD-003) predisposed to fatty liver haemorrhagic syndrome (FLHS). The first investigated the effect of adding a fatty liver supplement to the diet of laying hens prior to the onset of lay, and continuing either until peak production or throughout 39 weeks into lay. The second experiment, lasting 9 months into lay, investigated the effect of adding a fatty liver supplement, with or without 100 g/kg dietary ground flaxseed, to the diet. Body weight, feed intake, plasma triglycerides (in experiment 2) and egg production were measured throughout the experiment. Liver weight, liver fat content, liver malondialdehyde (MDA) content and liver haemorrhage score and fatty acid content of liver fat (in experiment 2) were measured at the end of each experiment. 2. In experiment 1, hens given diets containing the fatty liver supplement had higher egg production and eggshell strength, but there was no difference in liver parameters including MDA content or haemorrhage score compared with controls. 3. At the end of experiment 2, hens on 100 g/kg flaxseed diets had lower body weight, liver weight, liver dry matter and fat content, and plasma triglyceride concentrations than hens given the control diets. 4. Liver haemorrhage score was positively correlated with liver weight, but not with liver fat content, plasma triglyceride concentration or liver MDA content. This suggests that reducing the liver lipid content or feeding fatty liver supplements may not be as effective in controlling FLHS as controlling the size of the liver.

Animal Feed↗
PubMed1977

Fatty liver induced in Zucker "fatty" (ff) rats by a semisynthetic diet rich in sucrose.

A new fatty liver model is described in which heredity plays a major role. A marked fatty liver develops when the homozygous mutant Zucker rat (ff or "fatty") is fed a semi-synthetic diet enriched in sucrose. Lean littermates do not develop fatty livers on this experimental diet. Even old ff rats do not develop fatty livers on chow; the experimental diet is required. The fatty liver is described, including light microscopic and preliminary electron microscopic observations.

Animals↗
PubMed1977

Fatty liver induced in Zucker "fatty" (ff) rats by a semisynthetic diet rich in sucrose.

A new fatty liver model is described in which heredity plays a major role. A marked fatty liver develops when the homozygous mutant Zucker rat (ff or "fatty") is fed a semisynthetic diet enriched in sucrose. Lean littermates do not develop fatty liver on this experimental diet. Even old ff rats do not develop fatty livers on chow; the experimental diet is required. The fatty liver is described, including light microscopic and preliminary electron microscopic observations.

Animals↗
PubMed2006

Current pharmacological treatment of nonalcoholic fatty liver.

Nonalcoholic fatty liver disease (NAFLD) is a frequent and potentially progressive chronic liver disease that occurs in subjects who do not abuse alcohol. NAFLD is often associated with obesity, metabolic syndrome and insulin resistance and its more aggressive form, nonalcoholic steatohepatitis (NASH) is a major cause of cryptogenic cirrhosis. NAFLD/NASH are commonly detected because of elevated serum aminotransferase levels, ultrasonographic fatty liver and, at liver histology, steatosis, inflammation, and occasionally fibrosis that may progress to cirrhosis. No established treatment exists for this potentially serious disorder. Current management of NAFLD/NASH is largely conservative and includes diet regimen, aerobic exercise, and interventions towards the associated metabolic abnormalities. The main concern is therefore to decrease liver steatosis and its progression toward steatohepatitis and fibrosis, and the risk of "cryptogenic" cirrhosis. Among the most promising medications, weight reducing drugs, insulin sensitizers and lipid-lowering agents, antioxidants, bile salts, co-factors increasing the mitochondrial transport of fatty acids are being considered. Among them, thiazolidinediones are the most promising drug family that act by activating PPARgamma nuclear receptors and by regulating both microsomal and peroxisomal lipid oxidative pathways. Pharmacological treatment of obesity and probiotics should be considered as potential therapeutic options. In this review, after summarizing the general background on fatty liver, the most current and attractive pharmacological approaches to the problem of NAFLD/NASH are discussed.

Anti-Obesity Agents↗
PubMed1983

[Nonalcoholic fatty liver hepatitis and fatty cirrhosis mimicking alcoholic liver diseases].

Non-alcoholic steatosis hepatitis and fatty cirrhosis represents an unfamiliar liver disease of yet unknown etiology, which is usually indistinguishable from alcoholic lesions by histological criteria. For the affected patients this means automatically the inappropriate assumption of hidden alcohol abuse. Out of 1467 liver biopsies during 1979 to 1982 we selected 25 patients (group I), who either denied alcohol intake or reported negligible consumption. None of them had taken steatogenous drugs or had been treated by jejuno-ileal bypass operation for morbid obesity. Nevertheless, in all cases liver biopsy demonstrated changes that were thought to be characteristic of alcoholic liver disease. This group was compared with an additional series of 25 patients (group II, selected out of 342 alcoholics), who admitted to a mean daily alcohol ingestion of 145 +/- 37 g. According to body weight, sex ratio, estimated degree of hepatocellular fat deposition and relation of steatosis hepatitis (n = 15) to fatty cirrhosis (n = 12) there were no differences between both groups. In contrast to the alcoholics (group II) significantly lower (p less than 0.001) values of serum gamma-glutamyltransferase (127 +/- 138 vs 669 +/- 588 U/l) and mean corpuscular erythrocyte volume (89 +/- 4,7 vs 102 +/- 7,8 fl) occurred among the abstinent patients (group I). However, the considerable overlap of measured values argued against a sufficiently discriminative function of both parameters. On the other hand, the serum SGOT/SGPT ratio (I: 1,0 +/- 0,4 vs II: 3,5 +/- 1,4) as well as the serum immunoglobulin-index IgG/IgA (I: 5,6 +/- 2,1 vs II: 2,7 +/- 0,7) allowed a more than 90% separation between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

Association of nonalcoholic fatty liver disease with type 2 diabetes: clinical features and independent risk factors in diabetic fatty liver patients.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLDéis a common chronic liver disease in China, of which diabetic fatty liver (DFLéaccounts for a large proportion in clinic. DFL is a disease without specific clinical features and lacking of confirmatory laboratory tests, and the etiology of hepatic steatosis remains poorly understood. The aim of this paper was to explore the clinical characteristics and to determine associated risk factors in type 2 diabetes patients with fatty liver. METHODS: A total of 166 patients, 53 in DFL group and 113 in NDFL (diabetes without fatty liverégroup participated in this study. Serum fasting blood glucose (FBG), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphate (AKP), gamma glutamyl transpeptidase (GGT), total cholesterol (TC), triglyceride (TG), high density lipoprotein-cholesterol (HDL-C)were measured in both groups. And these variables were analyzed by using Student's t test and logistic regression model. RESULTS: A progressive increase in the level of FBG, ALT, AST, AKP, GGT, TG (P < 0.05) and a decrease of HDL-C (P < 0.01) were observed from DFL group to NDFL group. And there was no statistical difference in the level of TC between the two groups. CONCLUSIONS: Dyslipidemia, dysglycemia and elevation of liver enzyme can be seen more frequently in the DFL patients than in the NDFL patients. The successive escalation of serum ALT and TG levels and the lower HDL-C level are the independent risk factors of DFL.

Aged↗
PubMed1995

[Atypical focal fatty liver].

Focal fatty liver disease can cause difficulties in the differential diagnosis by ultrasound, CT, and MRI. This case report describes the atypical findings of focal spared areas of fatty liver disease in association with inflammatory changes, which were thought to be malignant focal liver lesions.

Adult↗
PubMed2002

[Nonalcoholic fatty liver].

Nonalcoholic fatty liver disease (NAFLD) is most often associated with obesity, type II Diabetes mellitus, hyperlipidemia and chronic viral hepatitis C. The spectrum of changes encompasses fatty liver, steatohepatitis, liver fibrosis and cirrhosis. Most patients are asymptomatic. The aminotransferases are only slightly elevated (ALT > AST). Grade of inflammation and stage of fibrosis can be assessed accurately only by histologic examination of liver biopsy. In most cases prognosis is favourable but in a subgroup of patients NAFLD may progress to cirrhosis. Recent data suggest that up to 70% of cryptogenic cirrhoses are accounted for by nonalcoholic steatohepatitis. At the moment therapeutic modalities of proven value are not available.

Biopsy↗