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PubMed2003

Prevention of diet-induced fatty liver in experimental animals by the oral administration of a fatty acid bile acid conjugate (FABAC).

Fatty acid bile acid conjugates (FABACs) are a new family of synthetic molecules designed to solubilize biliary cholesterol. They were shown to prevent and dissolve cholesterol gallstones in inbred C57L/J mice fed a lithogenic, high-fat diet (HFD). In these mice, fatty liver was observed in the controls but not in the FABAC-treated ones. The present study was designed to study the effect of FABAC (arachidyl-amido-cholanoic acid) on diet-induced fatty liver in rats, hamsters, and mice. The fatty liver score (on a scale of 0-4 by light microscopy) was 4.0 in control hamsters and 0.3 in the FABAC-fed hamsters (P <.001). In mice it was 1.5 and 0.4, respectively (P <.01). The lipid/protein ratio in the liver was 1.3 +/- 0.44 (mg lipid/mg protein) in control rats and 0.66 +/- 0.04 in the FABAC group (P =.001) after 14 days. In hamsters it was 1.41 +/- 0.27 and 1.11 +/- 0.20, respectively (P =.03), after 21 days. In Imperial Charles River (ICR) mice the ratio was 0.34 +/- 0.10 and 0.17 +/- 0.07 (P =.03), respectively, after 24 days. Liver fat concentration, measured as mg lipid/g liver tissue, decreased similarly by FABAC feeding. The decrease in liver fat affected mainly the triglyceride levels. FABAC-fed animals gained weight similarly to the controls. Triglyceride absorption was unaffected by FABAC supplementation. In conclusion, oral FABAC therapy prevents/reduces the development of fatty liver in animals consuming a HFD.

Administration, Oral↗
PubMed2005

Plasma adiponectin is decreased in nonalcoholic fatty liver disease.

OBJECTIVES: Nonalcoholic fatty liver disease (NAFLD) is a major cause of liver-related morbidity and is frequently associated with obesity and metabolic syndrome. The recently discovered hormone adiponectin is produced by adipose tissue, and low plasma adiponectin is considered a key factor in the development of the insulin resistance underlying metabolic syndrome. Animal studies suggest that adiponectin may protect against non-alcoholic steatohepatitis, but direct evidence in humans is lacking. We therefore conducted this study to assess the relationship between plasma adiponectin and nonalcoholic fatty liver disease to explore its role in the pathogenesis of this disease. DESIGN AND METHODS: We measured plasma adiponectin and anthropometric, biochemical, hormonal and metabolic correlates in a group of 17 NAFLD patients with diagnosis confirmed by biopsy, and 20 controls with comparable age, body-mass index and sex. Furthermore we compared plasma adiponectin in patients with simple steatosis and steatohepatitis. RESULTS: Plasma adiponectin was significantly lower in NAFLD patients than controls (5.93+/-0.45 vs 15.67+/-1.60ng/ml). Moreover, NAFLD patients were significantly more insulin resistant while having similar serum leptin. Adiponectin was similar in simple steatosis and in steatohepatitis (6.16+/-0.78 vs 5.69+/-0.49ng/ml). An inverse correlation was observed between adiponectin and homeostatic model assessment (HOMA) of insulin resistance (P = 0.008), while adiponectin did not correlate with serum transaminases and lipid values. CONCLUSIONS: These data support a role for low circulating adiponectin in the pathogenesis of NAFLD and confirm the strict association between reduced adiponectin production by adipose tissue, NAFLD and insulin resistance.

Adiponectin↗
PubMed1991

[The differential diagnosis of liver metastasis and regional fatty liver: a comparison of CT and MRT].

Differentiation between liver metastases and local fat deposition may be difficult when using CT; the value of MRI was therefore investigated in 18 patients with metastases and ten patients with fat deposits. CT shows both lesions as similar hypodense areas. MRI, however, produces different appearances: T1- and 2-weighted images show marked differences in the signal arising from metastases, whereas local fat collections in both sequences differ little in their signal from normal liver. Quantitative MRI signal intensity of the two types of lesion were also different. Where the differentiation by CT may be difficult, it may be made with certainty by means of MRI.

Adult↗
PubMed2000

Mechanism of primary graft non-function in a rat model for fatty liver transplantation.

We established a fatty liver model in rat suitable for the model of human liver with steatosis by cholesterol enriched chow, and investigated the mechanism of primary graft non-function in fatty liver transplantation (LTx) using this model. Grafts with steatosis caused primary graft dysfunction after LTx following even short cold preservation; however, no significant difference was recognized in mitochondrial function of the graft during preservation. Morphological findings were not different at 1 h after reperfusion between non-steatotic and steatotic livers. Focal necrosis of hepatocytes was seen and the sinusoidal endothelial cells were injured 24 h after reperfusion. In addition, the fluidity of the plasma membrane decreased in fatty liver. Our results indicate that deterioration of sinusoidal endothelial cells after reperfusion causes graft dysfunction in LTx of steatotic liver.

Adenosine Triphosphate↗
PubMed2000

The effects of pantethine on fatty liver and fat distribution.

Although the prognosis of fatty liver depends on its causes, we feel from our clinical experience that fatty liver with hypertriglyceridemia has a good prognosis and responds well to treatment. In this study, 600 mg/day of pantethine was administered to 16 outpatients with fatty liver and hypertriglyceridemia for six months or longer to examine whether the drug improved fatty liver using abdominal plain computed tomography (CT). Nine of the 16-pantethine patients were no longer diagnosed as having fatty liver after the study period. An chi2 test indicated the significant disappearance of fatty liver. At the same time, the visceral fat calculated from the CT image passing the umbilical region was also significantly reduced. On the contrary, the subcutaneous fat area tended to increase, so the ratio of the visceral-to-subcutaneous fat area was reduced significantly. This indicates triglycerides may be pooled in the body as hepato-visceral fat and subcutaneous fat, and that pantethine may transfer fat from the liver and viscera to the subcutaneous tissue. This suggests that visceral fat deposition and fatty liver occurring with hypertriglyceridemia may have a common basis, probably excessive matrixes, and that pantethine may simultaneously improve the two conditions.

Abdomen↗
PubMed2003

Risk of cancer in patients hospitalized with fatty liver: a Danish cohort study.

GOALS: To examine the risk of cancer in patients with fatty liver. BACKGROUND: The relation between liver disease, including fatty liver, and cancer risk is poorly understood. STUDY: Using the population-based National Registry of Patients, we examined the incidence of cancer in 7,326 patients discharged with a diagnosis of fatty liver from a Danish hospital during 1977-1993. Patients with a prior diagnosis of liver cirrhosis were excluded. We identified cancers through the Danish Cancer Registry. The expected number of cancers was estimated from national age-, sex-, and site-specific incidence rates. RESULTS: Overall, 523 cancers were diagnosed during 47,594 person-years of follow-up, yielding a 1.7-fold increased risk (95% confidence interval, 1.6-1.9) compared with the Danish general population. The risk of primary liver cancer was markedly elevated in patients with alcoholic as well as nonalcoholic fatty liver with a standardized incidence ratio of 9.5 (95% confidence interval, 5.7-14.8) and 4.4 (95% confidence interval, 1.2-11.4), respectively. Patients with alcoholic fatty liver also had substantially increased risks of several types of cancer associated with alcohol and tobacco use (cancers of the lung, pharynx, larynx, esophagus, and stomach) and a moderately increased risk for cancers of the colon and breast. Among patients with nonalcoholic fatty liver, an increased risk of some alcohol- and tobacco-related cancers was seen, and there was also an increased risk of colon and pancreas cancer. CONCLUSIONS: Patients discharged with a diagnosis of fatty liver have an increased risk of cancer, in particular liver cancer, most prominently among patients with alcoholic fatty liver.

Age Distribution↗
PubMedDate not supplied

Diagnosis of fatty liver with MR imaging.

The diagnosis of fatty liver with magnetic resonance (MR) imaging was evaluated in experimental rat models of simple fatty infiltration and fatty liver with hepatocellular injury. T1 and T2 were measured ex vivo and correlated with the histologic degree of fatty infiltration. Enhancement of fatty liver with four different cells-specific contrast agents was studied with ex vivo relaxometry and in vivo MR imaging. Quantitative analysis of conventional and chemical shift MR images was correlated with biochemically determined fat content of the liver. Diet-induced simple fatty infiltration of the liver caused a decrease in T1 of 15%, whereas the T1 of L-ethionine-induced fatty liver with hepatocellular injury increased by 12%. T2 showed a positive correlation with the degree of fatty infiltration in both models. Cell-specific hepatobiliary contrast agents showed the same liver uptake and relaxation enhancement in fatty livers as in normal livers. Conventional T1-weighted images and chemical shift images showed good correlation (r = .83 and .80, respectively) between signal intensity and the degree of fatty infiltration. However, only chemical shift imaging was reliable in the diagnosis of fatty liver.

Acetates↗
PubMed1990

[Conformational changes of rat liver fatty acid binding protein induced by long chain fatty acid].

Rat Liver fatty acid binding protein (FABP) has been purified to homogeneity by the procedures including Sephadex G-100 and DEAE-cellulose column chromatography. FABP was resolved into two peaks of A and B by DEAE-cellulose column chromatography. Each of these fractions exhibited apparent homogeneity upon polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate with a molecular weight of 16,000 daltons and amino acid analysis of these fractions has revealed that they are identical protein. However, upon isoelectric focusing on polyacrylamide gel, the isoelectric (pl) points were differed considerably showing microheterogeneity. In the present investigation, one isoform (pl = 5.0) of FABP was purified by a successive DEAE-cellulose column chromatography and used for the subsequent experiments of fatty acyl-protein interactions. When the final FABP preparation was partly freed of fatty acids by a mild delipidation technique using Lipidex, the pl shifted toward higher regions of 7.0. However, the pl of the delipidated FABP turned to the original 7.0 by recombining fatty acids. On the other hand, the secondary and tertiary structures were also significantly changed by delipidization, which have been demonstrated by circular dichroism (CD) and nuclear magnetic resonance (1H-NMR) spectroscopy. Furthermore the structural properties of the delipidated FABP also could be restored by recombining fatty acid. These findings suggested that the weakly bound fatty acids are responsible for the functional capacity of the FABP by virtue of changing the protein conformation.

Animals↗
PubMed2003

Plasma lipid parameters in patients with alcoholic fatty liver after treatment with essential phospholipids.

BACKGROUND: Fatty liver is the earliest and most common response to alcohol. The accumulation of lipid particles in hepatocytes alters the ultrastructure of cellular membranes. The purpose of our study was to investigate the effect of the administration of essential phospholipids on plasma lipid parameters in patients with alcoholic fatty liver. METHODS: Our open clinical trial was performed in patients suffering from alcoholic fatty liver. The investigated group consisted of 29 patients. Two capsules of Essentiale forte were administered 3 times daily for 3 months. Individual biochemical parameters were examined each month. Values of total cholesterol, HDL- and LDL-cholesterol, triacylglycerols, apoprotein A and B were determined. RESULTS: The therapy with essential phospholipids had positive effects on the parameters of hepatocyte integrity. The levels of total cholesterol, triacylglycerols and apoprotein B were significantly higher in patients with fatty liver than in the controls. The concentration of HDL-cholesterol was also higher before the therapy than in the control group. There was no difference in levels of apoprotein A and LDL-cholesterol between the patients and the controls. There was no significant therapeutic effect on plasma lipid parameters in the group of patients with fatty liver. CONCLUSIONS: The effects of treatment of alcoholic fatty liver with essential phospholipids were studied. The therapy had positive effects on the parameters of hepatocyte integrity. There was no significant therapeutic effect of the therapy on plasma lipid parameters. (Tab. 2, Fig. 1, Ref. 20).

Adult↗
PubMed1999

Experimental study on preservation of rat fatty liver.

OBJECTIVE: To investigate the effects of cold preservation on rat fatty liver. METHODS: We observed the changes of portal perfusion pressure, endothelin-1, enzymes release in the effluent and mortality of sinusoid lining cell after 0h, 6h, or 12h preservation respectively and a subsequent 30 min reperfusion in rat fatty liver groups and control groups by using isolated perfused rat liver model. And we compared fatty liver groups with control groups by these indices. RESULTS: There was no obvious difference between mildly fatty liver group and control group after long time (12h) preservation, between moderately fatty liver group and control group after short time (6h) preservation, between severely fatty liver group and control group without preservation (0h), while preservation reperfusion injury was more severe in moderately fatty liver group than in control group after long time (12h) preservation and in severely fatty liver group than in control group after short time (6h) preservation. CONCLUSIONS: The authors suggested that a mildly fatty liver donor could be used in the same way as nonfatty liver and a moderately fatty liver donor could be used depending on the time of preservation and the balance of the emergent needs of recipient and donor organ supply, while severely fatty liver donor should be discarded without hesitation.

Animals↗
PubMed1992

Resistance to ketosis in moderately obese patients: influence of fatty liver.

To elucidate whether the presence of fatty liver influences ketogenesis in obesity, the metabolic and hormonal changes in basal and low-dose epinephrine (EPI)-stimulated states were studied in 12 obese patients (OB) with normal glucose tolerance, consisting of 6 without fatty liver (OBN) and 6 with fatty liver (OBF). In the basal state, the total ketone body (TKB) concentration and the TKB to free fatty acid (FFA) ratio were significantly (p < 0.01) lower in the OBF than in the OBN group, despite elevated, but comparable, FFA levels in both groups. The basal FFA level and the TKB/FFA ratio correlated with the degree of fatty liver (p < 0.05-0.01). EPI infusion resulted in accelerated lipolysis and diminished FFA-induced ketogenesis, similar to the findings of the basal data. These results suggest that fatty liver per se is related to diminished FFA-induced ketogenesis, leading to resistance to ketosis in obesity.

3-Hydroxybutyric Acid↗
PubMed1988

Biochemical changes associated with the fatty liver syndrome in cows.

There were significant changes in enzyme activities and concentrations of metabolites in the blood and liver of cows with fatty livers when compared to normal cows. Blood and liver samples were taken from cows at the abattoir immediately after slaughter. The liver was checked for pathological signs and the samples were divided according to the degree of fatty changes. Three groups were studied: controls showing no gross pathological signs, mild fatty infiltration and severe infiltration. In cows with fatty liver, there were significant increases in the serum activities of isocitric dehydrogenase (ICDH), glucose-6-phosphate dehydrogenase (G6PDH), glutamic dehydrogenase (GLDH), lactic dehydrogenase (LDH), malic dehydrogenase (MDH), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and acid phosphatase (ACP). In the fatty liver, the activities of the enzymes, ICDH, G6PDH, LDH, MDH, ALP and malic enzyme (ME) were significantly higher, while sorbitol dehydrogenase (SDH) was significantly lower. While serum total lipid decreased, the opposite was seen in the liver with higher lipid content, mainly due to triglycerides and cholesterol esters. The significant increases in the NADPH generating enzymes ME, ICDH, G6PDH and MDH, which are required for fatty acid synthesis, suggest that the lipids accumulated in the liver are not only of extrahepatic origin, mobilized into the liver, but also arise from increased lipid synthesis in the liver which is induced during the laying down of fat in the liver. Measurement of the serum NADPH generating enzymes may serve as a useful biochemical test specific for fatty liver in cows.

Alanine Transaminase↗
PubMed2004

Role of oxidative stress in the increased activation of signal transducers and activators of transcription-3 in the fatty livers of obese Zucker rats.

BACKGROUND: Fatty livers have chronic oxidative stress, which could activate several transcription factors. We hypothesized that fatty livers of obese rats have increased activation of signal transducers and activators of transcription-1 and transcription-3 (Stat-1 and Stat-3) and that tocopherol treatment will decrease Stat activation. METHODS: Obese (Ob) and lean (Ln) Zucker rats with or without tocopherol treatment were used. Western blots of liver nuclear and cytoplasmic extracts to assess phosphorylated and total Stat-3 and tyrosine kinases Jak-2 and Tyk-2, immunohistochemistry to assess distribution of phosphoStat-3, and gel shift assays to assess Stat and nuclear factor kappa B binding were performed. Interleukin-6 serum levels and hepatic transcripts were determined by immunoassay and reverse polymerase chain reaction with Southern blotting, respectively. RESULTS: Livers of Ob animals had increased nuclear phosphoStat-3, decreased cytoplasmic Stat-3, and increased Stat-3 binding. Serum interleukin-6 was not measurable in either Ob or Ln animals and hepatic transcript levels were not significantly different. Tocopherol administration decreased nuclear phosphoStat-3, increased cytoplasmic Stat-3, and decreased Stat-3 binding activity. CONCLUSIONS: Chronic oxidative stress in fatty livers is associated with increased Stat-3 activation and decreased cytosolic Stat-3. Tocopherol treatment decreases Stat-3 activation and increases cytosolic Stat-3. Tocopherol-induced changes in Stat-3 may play a role in its beneficial effects in hepatic ischemia in fatty livers.

Animals↗
PubMed2005

The metabolic syndrome as a predictor of nonalcoholic fatty liver disease.

BACKGROUND: The frequent association of nonalcoholic fatty liver disease with components of the metabolic syndrome such as obesity, hyperglycemia, dyslipidemia, and hypertension is well known. However, no prospective study has examined the role of the metabolic syndrome in the development of this disease. OBJECTIVE: To characterize the longitudinal relationship between the metabolic syndrome and nonalcoholic fatty liver disease. DESIGN: A prospective observational study. SETTING: A medical health checkup program in a general hospital. PARTICIPANTS: 4401 apparently healthy Japanese men and women, 21 to 80 years of age, with a mean body mass index (BMI) of 22.6 kg/m2 (SD, 3.0). MEASUREMENTS: Alcohol intake was assessed by using a questionnaire. Biochemical tests for liver and metabolic function and abdominal ultrasonography were done. Modified criteria of the National Cholesterol Education Program Adult Treatment Panel III were used to characterize the metabolic syndrome. RESULTS: At baseline, 812 of 4401 (18%) participants had nonalcoholic fatty liver disease. During the mean follow-up period of 414 days (SD, 128), the authors observed 308 new cases (10%) of nonalcoholic fatty liver disease among 3147 participants who were disease-free at baseline and who completed a second examination. Regression of nonalcoholic fatty liver disease was found in 113 (16%) of 704 participants who had the disease at baseline and who completed a second examination. Men and women who met the criteria for the metabolic syndrome at baseline were more likely to develop the disease during follow-up (adjusted odds ratio, 4.00 [95% CI, 2.63 to 6.08] and 11.20 [CI, 4.85 to 25.87], respectively). Nonalcoholic fatty liver disease was less likely to regress in those participants with the metabolic syndrome at baseline. LIMITATIONS: Ultrasonography may lead to an incorrect diagnosis of nonalcoholic fatty liver disease in 10% to 30% of cases and cannot distinguish steatohepatitis from simple steatosis. Self-reported alcohol intake may cause bias. Because all of the participants were Japanese, generalizability to non-Japanese populations is uncertain. CONCLUSIONS: The metabolic syndrome is a strong predictor of nonalcoholic fatty liver disease.

Adult↗
PubMed2003

Relationship between genetic polymorphism of cytochrome P450IIE1 and fatty liver.

AIM: To study the correlation between genetic polymorphism of cytochrome P450IIE1 (CYPIIE1) and fatty liver. METHODS: Peripheral blood mononuclear cells were collected in 56 patients with fatty liver, 26 patients without fatty liver and 20 normal controls. Then PCR-RFLP was used to analyze genetic polymorphism of CYPIIE1 in monocytes on the region of Pst I and Rsa I. RESULTS: The frequency of homozygotic C1 gene in patients with alcoholic fatty liver (28.6%), obese fatty liver (38.5%), or diabetic fatty liver (33.3%) was significantly lower than that of the corresponding patients without fatty liver (100%, 100% and 80% respectively), while the frequency of C2 genes, including C1/C2 and C2/C2, was significantly higher (71.4%/0%, 61.5%/0%, and 66.7%/20%) (P<0.01). The frequency distribution of the above genes of non-fatty liver patients (100%/0, 100%/0, and 80%/20%) was not significantly different from that of the normal controls (85%/15%) (P>0.05). CONCLUSION: The genetic polymorphism of CYPIIE1 on the position of Pst I and Rsa I is related to the susceptibility of fatty liver. Besides, C2 gene may play a key role in the pathogenesis of fatty liver.

Cytochrome P-450 CYP2E1↗
PubMed1977

Abnormal mitochondria in hepatocytes in human fatty liver.

Liver biopsies from fatty livers in thirty patients whose daily alcohol consumption was excessive, or they were in a diabetic state or overweight, and liver biopsies from seven control patients not presenting the above disorders, were studied by light microscopy 0.75 micronm EPON embedded, toluidine blue stained sections, and electron microscopy. Abnormal mitochondria were rarely found in normal liver tissue and, if present, they were found only in periportal hepatocytes. The frequency of hepatocytes containing abnormal mitochondria was significantly higher in fatty liver than in normal liver (p less than 0.01). These cells were usually localized periportally, practically never in the centre of the lobule (p less than 0.01). The occurrence of abnormal mitochondria was not correlated with the degree of steatosis, and the increase in number of abnormal mitochondria was equally high in alcoholists, diabetics, and overweight subjects. The ultrastructural appearance and the periportal localization suggest a hyperfunction of the mitochondria, which may prevent a development of steatosis in these areas.

Alcoholism↗
PubMed2006

Nonalcoholic fatty liver disease manifesting esophageal variceal bleeding.

Nonalcoholic fatty liver disease (NAFLD) is a fatty liver disease occurring in patients without alcohol consumption. It includes a broad spectrum of liver disease, from fatty infiltration, inflammation and fibrosis, to cirrhosis, usually having obesity, hyperlipidemia, and diabetes mellitus as its etiology. NAFLD-related cirrhosis has rarely been reported in Taiwan. We herein report a 41-year-old male patient with nonalcoholic fatty liver cirrhosis (NAFLC), with the first clinical manifestation being bleeding esophageal varices (EV). The patient was obese with diabetes mellitus, but without hyperlipidemia or any history of drinking alcohol. The laboratory tests, abdominal sonography, and computed tomography revealed a typical case of liver cirrhosis. The pan-endoscopy disclosed EV with red-color sign. EV ligation was performed successfully to stop the bleeding. When the patient was in a stabilized clinical condition, a liver biopsy showed a typical histologic finding of NAFLD. Most of the cases of NAFLC reported in the literature have silent signs and symptoms. Sudden onset of the EV as the first clinical manifestation, as in this case, is rare. This case reminds us that NAFLD may indeed induce severe liver impairment, such as liver cirrhosis. Liver biochemical tests and abdominal sonography should be considered in patients with overt obesity and diabetes.

Adult↗