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PubMed2001

Assessment of donor fatty livers for liver transplantation.

AIM: The effect of fatty liver on graft survival, especially with reference to macrovesicular and microvesicular steatosis, is still uncertain. This preliminarily study was designed to create a noninvasive method for the quantification of the hepatic fat content in vivo and to establish provisional criteria for the assessment of fatty donor livers before liver transplantation among transplant surgeons, radiologists, and pathologists. METHODS AND MATERIALS: Different degrees of rat fatty liver model were established by feeding rats a diet deficient in choline and methionine for different periods of time. Computed tomography (CT) with test tubes containing variable percentages of fat equivalent substance were used to assess the severity of fatty change of the rat liver. This was then correlated with the histological classification, level of hepatic enzymes, and graft survival. RESULTS: Linear correlation between the fat volume fraction added to the test tubes and CT density were found. The process of producing a fatty liver via diet alteration peaked at week 3. At this time hepatic enzymes, radiological fat content, and posttransplantation survival were worse (P=0.013), compared with other time points. Radiological assessment of fatty liver correlated well with survival and serum glutamic oxaloacetic transaminase and glutamic pyruvate transaminase levels. CONCLUSION: Severe microvesicular steatosis does not influence recipient survival, however, macrovesicular steatosis affects graft survival. Caliber CT is a practical and simple method that allows an accurate noninvasive quantitative assessment of hepatic fatty infiltration. It has potential to be a useful parameter for the assessment of donor livers for clinical liver transplantation.

Animals↗
PubMed1995

Prevalence of fatty liver in Japanese children and relationship to obesity. An epidemiological ultrasonographic survey.

The prevalence of fatty liver in children is unknown and its relationship to obesity is poorly defined. The present study of 810 northern Japanese children (4-12 years old) determined the prevalence of fatty liver in the pediatric population and its relationship to obesity. Diagnosis of fatty liver was based on established real-time ultrasonographic criteria. The overall prevalence of fatty liver was 2.6% and was higher for boys (3.4%) than for girls (1.8%), although not statistically significant (P = 0.15). Fatty liver was found in children as young as 6 years of age. There was no significant association between the prevalence of fatty liver and height (physical growth). There was a strong positive correlation between fatty liver prevalence and established obesity indices: Rohrer's Index--chi 2 linear trend = 59.2, P < 0.0001; body mass index--chi 2 linear trend = 91.6, P < 0.0001; and age-gender-adjusted Japanese standard index of weight for height--chi 2 linear trend = 93.2, P < 0.0001. However, direct measurement of abdominal subcutaneous fat thickness by ultrasonography was the best predictor of fatty liver: chi 2 linear trend = 159, P < 0.0001. These results indicate that fatty liver may develop very early in life, and there is a direct relationship between degree of obesity and fatty liver in children.

Body Height↗
PubMed2000

[Prevalence and factors associated to the presence of fatty liver in apparently healthy adult men].

BACKGROUND: Alcohol intake in one of the factors associated with fatty liver, although its contribution as well as other factors have not been completely established. Therefore the aim of this study was to assess the prevalence and associated factors for fatty liver diagnosed by ultrasonography. SUBJECTS AND METHODS: 1,801 presumably healthy male workers (age range 18-60 years). A complete physical and laboratory investigations, including HBsAg and anti-HCV antibodies, a detailed interview on alcohol intake, and an abdominal ultrasound examination were performed in all cases. Diagnosis of fatty liver was based on defined ultrasonographic criteria. RESULTS: Eighty eight cases were excluded because of the HBsAg or anti-HCV positivity or incomplete ultrasonography. Among the remaining 1,713 cases, 236 (13.8%; 12.2-15.4) had fatty liver. Logistic regression analysis disclosed age (RR: 1.04; CI 95%; 1.03-1.05), ethanol intake > 40 g/d (2.19; 1.81-2.65), gamma-glutamyl-transferase > 40 U/l (3.51; 2.95-4.18), body mass index > 30 (3.87; 3.22-4.66) and glycemia > 120 mg/dl (2.69; 1.85-3.90) as the risk factors for fatty liver. Fatty liver was present in 8.8% of cases who did not have obesity, diabetes or hypercholesterolemia. When the subjects with obesity, hyperglycemia or hypercholesterolemia were excluded, regression analysis confirmed age, ethanol intake and gamma-glutamyl-transferase as independent factors associated with fatty liver. CONCLUSIONS: Age, alcohol intake, obesity, and increased serum levels of glucose, cholesterol and gammaglutamyl transferase are the main factors associated with fatty liver in presumably healthy adult men.

Adolescent↗
PubMed1989

Clinical and pathophysiological aspects of fatty liver of unknown etiology in modern Japan.

Recently, fatty liver of unknown etiology has been increasing in number among relatively younger persons in Japan. The tendency is very likely related to drastic reformation of the standard of living with the height of economic prosperity due to industrial advances in Japan at present. On the basis of our own 392 patients with fatty liver of unknown etiology, in whom fatty liver could be confirmed laparoscopically and bioptically, clinical and pathophysiological aspects of fatty liver of unknown etiology have been into consideration. The clinical outline of the disease was stated in this paper.

Body Weight↗
PubMed1995

The relationship between serum transaminase activities and fatty liver in children with simple obesity.

To determine hepatic diseases in obese children, biochemically and histologically, 11 obese patients with abnormal serum transaminase activities were subjected to this study. Fat accumulation in the liver was semiquantitatively graded, and histologically the 11 patients were classified into four groups; fatty liver, fatty hepatitis, fatty fibrosis and fatty cirrhosis. All patients had fat deposition in liver specimens, the grade of which did not significantly correlate with the degree of obesity. The grade of fat deposition in the liver specimens also did not significantly correlate with either serum transaminase activities or GOT/GPT ratio. Five patients were grouped into the fatty liver group, three into the fatty hepatitis group, and the remaining three patients into the fatty fibrosis group. However, no significant differences were found among the three histologically classified groups in terms of serum transaminase activities or GOT/GPT ratio. The usefulness of serum transaminase activities and GOT/GPT ratio was limited in predicting the severity of fat deposition or histological abnormality in pediatric obese patients.

Adolescent↗
PubMed2006

Histological assessment of non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) is an important complication of the metabolic syndrome, which is becoming an increasingly common cause of chronic liver disease. Histological changes typically mainly affect perivenular regions of the liver parenchyma and include an overlapping spectrum of steatosis, steatohepatitis and persinusoidal or pericellular fibrosis, in some cases leading to cirrhosis. Once cirrhosis has developed, typical hepatocellular changes are often no longer conspicuous, leading to such cases being mistakenly diagnosed as 'cryptogenic'. Portal inflammation, ductular reaction and periportal fibrosis can also be seen as part of the morphological spectrum of NAFLD, particularly in the paediatric population. Hepatocellular carcinoma has also been described as a complication of NAFLD-associated cirrhosis. NAFLD is also an important cofactor in other chronic liver diseases, especially hepatitis C. Histological assessments have an important role to play in the diagnosis and management of NAFLD. These include making the potentially important distinction between simple steatosis and steatohepatitis and providing pointers to the aetiology, including cases where a dual pathology exists. A number of systems have been devised for grading and staging the severity of fatty liver disease. These require further evaluation, but have a potentially important role to play in determining prognosis and monitoring therapeutic responses.

Biopsy↗
PubMed1988

Dependence of lipid-lipoprotein metabolism on exercise intensity in experimental fatty liver rats.

To develop experimental fatty liver, Wistar male rats were fed a high fat, high cholesterol (Cho) diet for 6 weeks after which their diet was changed to standard chow. The animals were then divided by random selection into a sedentary group (SG) and four treadmill exercise groups for 6 weeks as follows: walking group (WG, 10 m/min, 60 min); low-speed running group (LRG, 20 m/min, 30 min); middle-speed running group (MRG, 30 m/min, 20 min) and high-speed running group (HRG, 40 m/min, 15 min). The serum concentration of very low density lipoprotein (VLDL) and low density lipoprotein (LDL)-Cho decreased, and high density lipoprotein (HDL)-Cho increased in WG compared with the other three exercise groups. Hepatic triglyceride (TG) was significantly lower (P less than 0.05) in WG than in SG. Hepatic Cho was lower in HRG than in the other three exercise groups, and Cho in the aortic wall was higher. The results suggest that light exercise, such as walking might be more beneficial to lipid-lipoprotein metabolism than strong exercise, such as high-speed running. This is consistent with suggestion that light exercise might be effective in clinical treatment for hyperlipidemia, arteriosclerosis or fatty liver.

Animals↗
PubMed2006

Crohn's disease-induced non-alcoholic fatty liver disease (NAFLD) sensitizes for severe acute hepatitis B infection and liver failure.

Non-alcoholic fatty liver disease (NAFLD) commonly is associated with chronic inflammatory bowel disease (CIBD) and usually is considered to be stable and benign. However, NAFLD -- and in particular its subset, non-alcoholic steatohepatitis (NASH) -- may lead to progressive liver disease. Moreover, NAFLD sensitizes the liver to injury and increases the risk of developing acute-on-chronic liver failure following a "third hit". We here present one patient with NASH, as probably induced by long-standing Crohn's disease in the absence of ethanol consumption or abuse. The patient acquired an acute HBV infection and died from complications. As based on the clinical and histological findings, Crohn's disease appears to be a risk factor for developing NAFLD and thus to contribute to the progression into NASH. In conclusion, we suggest that Crohn's disease-related NAFLD may increase the vulnerability of the liver, which indicates that patients with a known history of CIBD merit special attention.

Crohn Disease↗
PubMed2004

Increased prevalence of fatty liver in arterial hypertensive patients with normal liver enzymes: role of insulin resistance.

BACKGROUND: The conditions associated with fatty liver disease presenting with normal liver enzymes and the mechanism involved in its development remain to be fully elucidated. AIMS: The aim of the present study was to test the hypothesis that fatty liver with normal liver enzymes occurs more frequently in arterial hypertensive patients and to establish whether this condition is associated with insulin resistance. PATIENTS: A total of 55 non-obese, non-diabetic, non-heavy alcohol drinking patients with arterial hypertensive and normal liver enzymes and 55 sex and age matched healthy subjects were enrolled into the study. METHODS: Plasma metabolic parameters, body mass index, and the presence of fatty liver were investigated. Insulin resistance was estimated from plasma insulin and glucose as the homeostasis model assessment index. Stepwise logistic regression and multivariate regression analysis were used on the combined sample to identify variables independently associated with fatty liver and insulin resistance. RESULTS: Hypertensive patients had a significantly higher prevalence of fatty liver (30.9% v 12.7%; p<0.041), higher insulin resistance (mean 2.27 (SD 1.81) v 1.56 (0.70); p = 0.022), and slightly higher body mass index (24.9 (3.0) v 24.0 (2.2); p = 0.043) than controls. Multivariate logistic regression identified insulin resistance (odds ratio 1.66 (95% confidence interval (CI) 1.03-2.52)) and body mass index (OR 1.22 (95% CI 1.00-1.49)) as factors independently associated with fatty liver. Multivariate regression analysis showed insulin resistance to be predicted by alanine transaminase (p = 0.002), presence of arterial hypertension (p = 0.029), and body mass index (p = 0.048). CONCLUSION: The higher prevalence of non-alcoholic fatty liver in non-obese hypertensive patients with normal liver enzymes appears to be related to increases in insulin resistance and body weight.

Adult↗
PubMed2005

Uncoupling protein-2 and non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) has become the most common form of hepatic disorders in the developed world. NAFLD is part of the metabolic syndrome with insulin resistance as a primary underlying derangement. The natural history of NAFLD may extend from simple steatosis over steatohepatitis into cirrhosis and hepatocellular carcinoma. Among numerous factors shaping these transitions, uncoupling protein-2 (UCP2) may theoretically contribute to every stage of this disease. UCP2 is a recently identified fatty acid-responsive mitochondrial inner membrane carrier protein showing wide tissue distribution with a substantially increased presence in fatty liver. The biological functions of UCP2 are not fully elucidated and the greater part of our current knowledge has been obtained from animal experiments. These data suggest a role for UCP2 in lipid metabolism, mitochondrial bioenergetics, oxidative stress, apoptosis, and even carcinogenesis. Available evidence is reviewed and new concepts are considered to appraise the potential role of UCP2 in the pathogenesis of NAFLD.

Alcoholics Anonymous↗
PubMed2006

Liver mitochondrial dysfunction and oxidative stress in the pathogenesis of experimental nonalcoholic fatty liver disease.

Oxidative stress and hepatic mitochondria play a role in the pathogenesis of nonalcoholic fatty liver disease. The aim of the present study was to evaluate the role of hepatic mitochondrial dysfunction and oxidative stress in the pathogenesis of the disease. Fatty liver was induced in Wistar rats with a choline-deficient diet (CD; N = 7) or a high-fat diet enriched with PUFAs-omega-3 (H; N = 7) for 4 weeks. The control group (N = 7) was fed a standard diet. Liver mitochondrial oxidation and phosphorylation were measured polarographically and oxidative stress was estimated on the basis of malondialdehyde and glutathione concentrations. Moderate macrovacuolar liver steatosis was observed in the CD group and mild liver steatosis was observed in the periportal area in the H group. There was an increase in the oxygen consumption rate by liver mitochondria in respiratory state 4 (S4) and a decrease in respiratory control rate (RCR) in the CD group (S4: 32.70 +/- 3.35; RCR: 2.55 +/- 0.15 ng atoms of O2 min-1 mg protein-1) when compared to the H and control groups (S4: 23.09 +/- 1.53, 17.04 +/- 2.03, RCR: 3.15 +/- 0.15, 3.68 +/- 0.15 ng atoms of O2 min-1 mg protein-1, respectively), P < 0.05. Hepatic lipoperoxide concentrations were significantly increased and the concentration of reduced glutathione was significantly reduced in the CD group. A choline-deficient diet causes moderate steatosis with disruption of liver mitochondrial function and increased oxidative stress. These data suggest that lipid peroxidation products can impair the flow of electrons along the respiratory chain, causing overreduction of respiratory chain components and enhanced mitochondrial reactive oxygen species. These findings are important in the pathogenesis of nonalcoholic fatty liver disease.

Animals↗
PubMed1990

Liver fatty acid-binding protein: a marker for studying cellular differentiation in gut epithelial neoplasms.

Human liver fatty acid binding protein is a 127 residue cytoplasmic protein synthesized in liver and in the intestinal epithelium. Previous studies of normal and transgenic mice indicated that the liver fatty acid-binding protein gene is a sensitive marker of enterocytic differentiation. This study shows the use of immunohistochemical methods to examine liver fatty acid-binding protein gene expression in normal human colonic epithelium, colonic villoglandular adenomas, nonmucinous and mucinous adenocarcinomas, and several types of noncolonic epithelial neoplasms. Cells containing liver fatty acid-binding protein were found in normal colonic epithelium, in two thirds of colorectal villoglandular adenomas and nonmucinous adenocarcinomas, and in one third of mucinous adenocarcinomas but not in noncolonic, nonhepatic carcinomas. All liver fatty acid-binding protein-positive colonic adenomas and adenocarcinomas contained patches of immunoreactive cells distributed among histologically identical patches of cells without liver fatty acid-binding protein immunoreactivity. This "mosaicism" was also found in metastases from liver fatty acid-binding protein-positive colonic adenocarcinomas. Immunostaining of these liver fatty acid-binding protein-positive tissues for carcinoembryonic antigen did not show a mosaic cellular pattern in its expression. These data suggest that within a given neoplasm, differences exist in the differentiation programs of monoclonally-derived, malignant colonic epithelial cells and that liver fatty acid-binding protein is a useful marker for operationally defining these subpopulations. Liver fatty acid-binding protein is also a potentially useful diagnostic marker for colorectal and hepatic carcinomas.

Adenocarcinoma↗
PubMedDate not supplied

Fatty liver suppressed the angiogenesis in liver metastatic lesions.

BACKGROUND/AIMS: We have demonstrated that colorectal cancer with fatty liver had few liver metastases clinically as well as experimentally. In this study, to clarify why colorectal cancer with fatty liver had few liver metastases, we focused on the angiogenesis of carcinomas. METHODOLOGY: The rat colon cancer cells (RCN-9) were injected into 40 rats (the fatty liver group = FL group includes 20 rats, the non-fatty liver group = NFL group includes 20 rats). In each group, the PyNPase (pyrimidine nucleoside phosphorylase) activity in the metastatic lesion of the liver was examined using the high-performance liquid chromatographic method. In addition, the microvessel density in the metastatic lesion of the liver was assessed by Von Willebrand factor-related antigen immunostaining. RESULTS: 1) The PyNPase activity in the FL group was 33.34 +/- 6.27 (microgram FU/mg protein/hr), which was significantly lower than that of the NFL group (49.30 +/- 14.82) (P = 0.0021). 2) Microvessel density in the FL group was 1.845 +/- 0.357 (%), while that in the NFL group was 2.777 +/- 1.371 (%). The microvessel density of the FL group was significantly lower than that of the NFL group (P = 0.0365). 3) The regression coefficient between PyNPase activity and microvessel density was 0.480, which indicated a significant correlation (P = 0.0098). CONCLUSIONS: We think that, in colorectal carcinomas with fatty liver, the decreased activity of PyNPase and the decreased neovascularization in the metastatic lesion are closely related to fewer liver metastasis compared with colorectal cancer patients without fatty liver.

Animals↗
PubMed1986

Subcapsular hematoma in fatty liver of pregnancy.

A case of fatty liver of pregnancy with subcapsular hematoma of the liver caused by intravenous heparin treatment is reported. The heparin was given for the thrombophlebitis of leg veins. The patient expired suddenly as a result of rupture of the subcapsular hematoma of the liver causing massive intraperitoneal hemorrhage. The pathophysiology and complications of the fatty liver of pregnancy are discussed.

Adult↗
PubMed2005

[Therapeutic options for nonalcoholic fatty liver disease and steatohepatitis].

Nonalcoholic fatty liver disease (NAFLD) is increasingly recognized as one of the most common causes of chronic liver damage in the western world. It is strongly associated with insulin resistance, obesity and other features of the metabolic syndrome. The entity NAFLD embraces a clinical spectrum from benign steatosis over steatohepatitis to hepatic cirrhosis with its complications liver failure and hepatocellular carcinoma. Treatment is currently based on prescriptive diet and physical exercise. A well-defined pharmacotherapy of NAFLD still remains to be established due to the lack of randomized, controlled trials. Yet, for several drugs such as Metformin and Thiazolidinediones, smaller trials report promising results.

Diet Therapy↗
PubMedDate not supplied

The association of dehydroepiandrosterone, obesity, waist-hip ratio and insulin resistance with fatty liver in postmenopausal women--a hyperinsulinemic euglycemic insulin clamp study.

BACKGROUND/AIMS: The relationship between insulin resistance and the occurrence of fatty acid has been documented. Recently DHEA (dehydroepiandrosterone) was shown to have a protective effect against development of fatty liver in rats. We aimed to investigate the association of nonalcoholic fatty liver and serum levels of DHEA, obesity, fat distribution and insulin resistance and to evaluate the effect of DHEA on fatty liver, obesity and insulin resistance. METHODOLOGY: Thirteen postmenopausal women with nonalcoholic fatty liver and 14 postmenopausal women with normal liver histology were included into the study. Body mass index, waist-hip ratio, serum DHEA, DHEAS, triglyceride, cholesterol levels and insulin resistance were determined. Fatty liver was determined by ultrasound and established by liver biopsy and histology. Hyperinsulinemic euglycemic clamp studies were performed. RESULTS: The subjects in both groups were age matched (p > 0.05). Body mass index showed obesity in patients with fatty liver but not in control group (p = 0.01). Central obesity was present in women with fatty liver (p = 0.039). As expected, insulin resistance was significantly present in patients with fatty liver (p = 0.001). DHEA and DHEAS levels of women with fatty liver were greater than those of control group (p1 = 0.001 and p2 = 0.0001, respectively). DHEA and DHEAS were positively correlated with both body mass index and waist-hip ratio. However, glucose disposal rate was inversely and significantly correlated with DHEA and DHEAS levels. CONCLUSIONS: These data do not support the hypothesis that DHEA or DHEAS protect post-menopausal women against fatty liver, diabetes and obesity. Indeed, DHEA and DHEAS may be the cause of fatty liver, obesity (especially abdominal obesity) and diabetes in estrogen-deficient women.

Blood Glucose↗
PubMed2005

Obesity, fatty liver and liver cancer.

BACKGROUND: It has been suggested that obesity and fatty liver may be associated with the morbidity and mortality of liver cancer, and the early diagnosis and effective treatment of fatty liver coupled with liver cancer are supposed to improve the prognosis of obese patients. This review was attempted to understand the relationship between obesity, fatty liver and liver cancer. DATA RESOURCES: An English-language literature search using PUBMED (1990-2004) on obesity, fatty liver and liver cancer and other related articles in Chinese. RESULTS: Obesity is associated with the risk of death from all cancers and from cancers at individual sites including liver cancer, and it is an independent risk factor for hepatocellular carcinoma (HCC) in patients with alcoholic cirrhosis and cryptogenic cirrhosis. Because nonalcoholic steatohepatitis has been implicated as a major cause of cryptogenic cirrhosis, the development of HCC may be part of progressive nature of this condition. CONCLUSIONS: Obesity is associated with the incidence and mortality of HCC. More frequent surveillance for HCC may be warranted in obese patients with fatty liver and attempts should be made to interrupt the progression from simple hepatic steatosis to steatohepatitis, cirrhosis and ultimately HCC.

Adult↗