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PubMedDate not supplied

[Acute fatty liver of pregnancy. Three case reports].

The acute fatty liver of pregnancy is a specific disease of pregnancy. Its incidence is rare but prognosis is poor in complicated entities, and can compromise the foetal and maternal life. An early diagnosis of the illness and a multidisciplinary management based on uterine evacuation and an intensive medical care can improve the prognosis of the acute fatty liver of pregnancy (A.F.L.P). In hope to contribute at a better approach of this affection, the authors report their experience about 3 cases of A.F.L.P., collected in 1997.

Acute Disease↗
PubMed2002

[Relation of apolipoprotein E polymorphism to clinically diagnosed fatty liver disease].

BACKGROUND/AIMS: Apolipoprotein E (Apo E) is important in plasma lipid metabolism and is a component of several plasma lipoprotein-lipid particles. Three major Apo E isoforms are encoded by three common allelic forms, epsilon2, epsilon3, and epsilon4 at the APO E locus. The goal of this study was to examine the association between polymorphisms in the apolipoprotein E gene (APOE) and fatty liver disease. METHODS: We examined the distribution of APOE alleles from 116 fatty liver patients and 50 controls in Korea. RESULTS: The frequencies of APOE alleles in fatty liver patients were 6.5% in epsilon2, 85.7% in epsilon3 and 7.8% in epsilon4. The corresponding frequencies in control subjects were 4.0% in epsilon2, 91.0% in epsilon3 and 5.0% in epsilon4. There were no significant differences in the distribution of APOE genotypes between fatty liver patients and controls. APOE epsilon2 and epsilon4 allele frequencies in fatty liver patients were more than those in controls. However, there was no significant differences in APOE epsilon2 and epsilon4 allele frequencies. CONCLUSIONS: These results suggest that APOE alleles seem not to be directly associated with the pathogenesis of fatty liver disease.

Adult↗
PubMed1991

Hypoechoic lesions in fatty liver. Quantitative study by histomorphometry.

Ten patients with fatty liver changes were subjected to liver biopsies. In seven, ultrasonography showed focal hypoechogenicity within a "bright" liver, generally interpreted as focal sparing. Three patients had hyperechoic areas surrounded by "normal" parenchyma usually felt to represent local fat accumulation without diffuse involvement. Morphometric analysis was used to determine the total area occupied by fat (area density) and the number of lipid droplets (numerical density) per microscopic field in lesional and perilesional specimens. Compared with respective perilesional values, hypoechoic lesional numerical densities were significantly lower in 6 of 7 patients; the three hyperechoic samples had significantly higher values. In most cases, lesional and perilesional area densities were not significantly different. These hypoechoic focal lesions are believed to be merely areas in which a similar quantity of fat is contained in fewer droplets, and focal hyperechogenicity is believed to result from a larger number of fat-filled vacuoles with respect to that of the surrounding parenchyma. Variation in the number of solid-liquid interfaces causes the ultrasonic contrast between these lesions and the similarity fatty liver parenchyma surrounding them.

Biopsy, Needle↗
PubMed2001

[Studies on fatty liver, blood glucose and related factors in simple obese children].

OBJECTIVE: To study the prevalence of fatty liver, blood glucose and related factors in simple obese children. METHODS: Their liver was scanned with B-type ultrasound and fasting blood glucose (with a microassay glucometer), as well as other related morphological and functional indices, were measured in 62 children aged 8 to 11 years, including 32 obese ones and 30 control ones. RESULTS: Prevalence of fatty liver in obese and control groups was 93.8% and 10%, respectively, with very statistically significant difference (P < 0.01). Blood glucose level in obese and control groups was 5.42 mmol/L and 5.54 mmol/L, respectively, with statistically significant difference (P < 0.05). Proportion of children with normal cardiac function was 62.5% and 93.3%, respectively, in obese and control groups, with significant difference (P < 0.05). The prevalence of fatty liver correlated positively with skin-fold thickness, waist to hip ratio (WHR) and body mass index (BMI), with coefficients of correlation of 0.8786, 0.6256 and 0.8454, respectively (P < 0.01). Blood glucose correlated with skin-fold thickness and BMI positively, with coefficients of correlation of 0.3403 and 0.3155, respectively (P < 0.05). Regression analysis showed that skin-fold thickness and WHR were major risk factor for fatty liver and skin-fold thickness was major risk factor for high blood glucose. CONCLUSIONS: Simple obesity could cause damage to the liver, glucose metabolism and cardiac function in children, forming the potential risk factors for cardiovascular diseases, diabetes and disturbance of lipid metabolism in adults.

Blood Glucose↗
PubMed2004

Effect of body mass index on nonalcoholic fatty liver disease in patients undergoing minimally invasive bariatric surgery.

The risk factors for nonalcoholic fatty liver disease in patients undergoing bariatric surgery are under study. We wanted to determine the correlation between nonalcoholic fatty liver disease and patient factors such as obesity and liver function tests. A retrospective analysis was performed on 177 nonalcoholic morbidly obese patients who underwent laparoscopic Roux-en-Y gastric bypass with liver biopsy, to identify risk factors for nonalcoholic fatty liver disease. The histologic grade of liver disease was compared with preoperative body mass index, age, and liver function tests. Simple steatosis and steatohepatitis were present in 90% and 42% of patients, respectively. Elevated transaminase levels were an independent risk for liver disease. Body mass index and liver disease were not correlated with univariate analysis. Regression analysis performed on age, body mass index, and liver disease demonstrated that the risk for liver disease increased with body mass index in the younger (<35 years old) age group and decreased with body mass index in the older (>45 years old) age group. There was a high incidence of steatosis and steatohepatitis in these nonalcoholic bariatric patients, and elevated transaminase level was indicative of disease. Body mass index was a positive risk factor for liver disease in younger patients but a negative risk factor in the older patients.

Adult↗
PubMed2005

Polymorphism of the PEMT gene and susceptibility to nonalcoholic fatty liver disease (NAFLD).

Phosphatidylethanolamine N-methyltransferase (PEMT) catalyzes phosphatidylcholine synthesis. PEMT knockout mice have fatty livers, and it is possible that, in humans, nonalcoholic fatty liver disease (NAFLD) might be associated with PEMT gene polymorphisms. DNA samples from 59 humans without fatty liver and from 28 humans with NAFLD were genotyped for a single nucleotide polymorphism in exon 8 of PEMT, which leads to a V175M substitution. V175M is a loss of function mutation, as determined by transiently transfecting McArdle-RH7777 cells with constructs of wild-type PEMT open reading frame or the V175M mutant. Met/Met at residue 175 (loss of function SNP) occurred in 67.9% of the NAFLD subjects and in only 40.7% of control subjects (P<0.03). For the first time we report that a polymorphism of the human PEMT gene (V175M) is associated with diminished activity and may confer susceptibility to NAFLD.

Adolescent↗
PubMed2006

In vivo assessment of liver cell apoptosis as a novel biomarker of disease severity in nonalcoholic fatty liver disease.

In patients with nonalcoholic fatty liver disease (NAFLD), a liver biopsy remains the only reliable way to differentiate simple steatosis from nonalcoholic steatohepatitis (NASH). Noninvasive methods are urgently needed. Increasing evidence suggests hepatocyte apoptosis is a key mediator of liver injury in NAFLD. The aim of this study was to quantify hepatocyte apoptosis in plasma from patients with NAFLD and correlate it with histological severity. Plasma was obtained from 44 consecutive patients with suspected NAFLD at the time of liver biopsy. Histology was assessed blindly. Caspase-3-generated cytokeratin-18 fragments were measured in situ via immunohistochemistry and in vivo using a novel enzyme-linked immunosorbent assay. Plasma cytokeratin-18 fragments were markedly increased in patients with NASH compared with patients with simple steatosis or normal biopsies (median [interquartile range]: 765.7 U/L [479.6-991.1], 202.4 U/L [160.4-258.2], 215.5 U/L [150.2-296.2], respectively; P < .001). Cytokeratin-18 fragment levels independently predicted NASH (OR 1.95; 95% CI 1.18-3.22; P = .009 for every 50 U/L increase). A cutoff value of 395 U/L calculated using the receiver operating characteristic curve approach showed a specificity of 99.9%, a sensitivity of 85.7%, and positive and negative predictive values of 99.9% and 85.7%, respectively, for the diagnosis of NASH. In conclusion, these findings strongly suggest that determination of hepatocyte caspase activation in the blood is a strong and independent predictor of NASH in human subjects. These data highlight the potential usefulness of this test as a noninvasive diagnostic means of determining histological disease severity in patients with NAFLD.

Apoptosis↗
PubMed2001

[Different serum lipid adjustment drugs for the treatment of hyperlipidemic fatty liver].

OBJECTIVE: To research the effect of different serum lipid adjustment drugs, Simvastatin and Fenofibrate, on hyperlipidemic fatty liver. METHODS: The rat models of hyperlipidemic fatty liver induced by high fat diet were treated with Fenofibrate and Simvastatin respectively to investigate the change of the liver index, liver function, the serum and liver lipid, MDA, and pathologic histology. RESULTS: The liver index and the content of triglyceride (TC1.80 +/-0.20/2.10+/-0.33), total cholesterol (TG 0.76+/-0.18/1.09+/-0.31), MDA both in the serum and the liver in the model group were significantly higher than those in control group. Slight or moderate hepatic steatosis was observed in model group. Fenofibrate decreased serum triglyceride, total cholesterol, and MDA both in serum and liver significantly, but increased the ALT, ALP, liver index, liver lipids, and finally leading to severe hepatic steatosis. Simvastatin lowered the level of lipid and MDA both in serum and liver, and liver histology was improved nearly to normal. Moreover, little side effect on the liver was observed. CONCLUSIONS: Simvastatin can be applied for prevention and treatment of hyperlipidemic fatty liver safely and effectively, while Fenofibrate can not.

Animals↗
PubMed1989

Plasma lipoproteins in dairy cows with naturally occurring severe fatty liver: evidence of alteration in the distribution of apo A-I-containing lipoproteins.

The relationships between fatty liver in dairy cows and reduced levels of plasma lipoproteins, and particularly of low density lipoproteins (LDL), has been previously described. Since electrophoretic heterogeneity of ultracentrifugally isolated LDL (d, 1.006-1.063 g/ml) has been found, the exact nature of this reduction in cows with fatty liver was investigated. Lipoproteins from control and severely afflicted animals were isolated by ultracentrifugation and affinity chromatography on heparin-Sepharose CL 6 B. Gradient gel electrophoresis of lipoproteins on 4-30% gels and an immunolocalization study of apoprotein A-I (apo A-I) showed that control animals have two subpopulations of apo A-I-containing particles with a mean radius of 6.52 and 5.05 nm. In the fatty liver cows, the former was clearly shifted toward smaller particles. We concluded that the depressed level and compositional modifications of LDL in severe fatty liver cows result from a decrease in the oversized apo A-I-containing lipoproteins which can be isolated in the LDL density range. This could stem from the decreased supply of triglyceride-rich lipoprotein surface components for the production of these lipoproteins. The modifications can be plausibly explained by a reduced synthesis or secretion of very low density lipoproteins (VLDL) by the liver.

Animals↗
PubMedDate not supplied

Efficacy of sodium borate in the prevention of fatty liver in dairy cows.

The effects of sodium borate (100 mg/kg body weight, p.o., 15 days) from a month before expected calving until a month after calving were evaluated in dairy cows susceptible to fatty liver. Cows received either sodium borate (n = 13) or no treatment (n = 10). All cows had mild fatty livers and increased plasma triglycerides and very low density lipoprotein (VLDL) concentrations at the beginning of the experiment. The control group of cows developed significant fatty liver after calving, and 2 of them had severe fatty liver associated with clinical and biochemical abnormalities. There were no clinicopathological signs related to sodium borate administration. Serum triglycerides and VLDL concentrations before calving decreased significantly at calving and after calving in controls, and they were within the normal range only after calving. There were significant alterations during the experiment in some hematological and chemical variables between groups, within period, but they were within the normal range. Unlike treated cows, serum triglycerides and VLDL concentrations correlated with liver fat content after calving in untreated cows. Our results document that sodium borate decreases the degree of fatty liver in dairy cows during early lactation.

Animals↗
PubMed2004

Portal fibrosis and hepatic steatosis in morbidly obese subjects: A spectrum of nonalcoholic fatty liver disease.

Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease (NAFLD) that can lead to hepatic fibrosis and cirrhosis. Portal fibrosis in the absence of NASH, called isolated portal fibrosis (IPF), has received less attention and has not been classified as a spectrum of NAFLD. The aims of this study were to determine the prevalence of IPF in subjects undergoing gastric bypass surgery, to identify biochemical variables associated with IPF, and to assess the metabolic syndrome as defined by the AdultTreatment Panel III criteria. We analyzed liver biopsies from 195 morbidly obese subjects after excluding all other causes of liver disease. The prevalence of fatty liver (FL) only, IPF, and NASH was 30.3%, 33.3%, and 36.4%, respectively. Several biochemical parameters significantly trended across the 3 groups, with IPF falling between FL and NASH. Hyperglycemia was the only metabolic parameter associated with NASH (OR, 5.4; 95% CI, 2.4-12; P < .0001) and IPF (OR, 2.8; 95% CI, 1.2-6.5; P = .01). Subjects with diabetes had the greatest risk for NASH (OR, 8; 95% CI, 3.3-19.7; P < .0001) and IPF (OR, 4.3; 95% CI, 1.6-11.6; P = .003). The metabolic syndrome was identified in 78.5% of subjects, and a significant trend for the number of metabolic criteria was observed across the spectrum of FL, IPF, and NASH. In conclusion, a significant subset of morbidly obese individuals has portal fibrosis in the absence of NASH that is associated with glycemic dysregulation. Therefore, IPF should be considered a spectrum of NAFLD that may prelude NASH in morbid obesity.

Adult↗
PubMed2005

[Study on therapeutic effects of metformin on rat fatty livers induced by high fat feeding].

OBJECTIVES: To explore the therapeutic effects of metformin on rat fatty livers induced by high fat feeding. METHODS: A fatty liver model was established by feeding rats with a high caloric laboratory chow for 12 weeks, then the rats were randomly divided into three groups, i.e. model control group, metformin group and dietary treatment group. A normal control group was organized at the same time. The rats of the metformin group were given metformin 156 mg/kg/d while the other groups were given distilled water of the same volume by stomach feeding. The model control group rats were fed with high caloric laboratory chow while other groups were fed a normal diet. After four weeks, all the animals were sacrificed. Liver index (liver/body weight ratio), serum activities of liver-associated enzymes, blood lipids, liver triglycerides, fasting blood glucose, fasting plasma insulin, HOMA insulin resistance index (HOMA-IR), and the liver histology of rats of all groups were assayed. RESULTS: The body weight, liver index, serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT), total cholesterol (TC), triglycerides (TG) and liver triglycerides in the model group increased significantly, while HDL-cholesterol concentration decreased significantly. Fasting blood glucose, fasting plasma insulin and HOMA-IR showed an increasing tendency, but there was no significant difference of those indexes among the three groups. The liver histology in the model group showed moderate to severe steatosis, mainly as macro vesicle steatosis, lobular inflammatory, cell infiltration and necrosis. Compared with the model group, the levels of body weight, liver index, serum ALT, ALP, TC, TG and liver triglycerides in the metformin group were significantly lower and were similar to those of the normal group, while their HDL-cholesterol concentration was significantly higher. The liver histology in the metformin group was nearly normal. In the dietary treatment group, hyperlipidemia persisted, although liver index and GGT were lower and the liver histology changes were somewhat milder. CONCLUSION: It is suggestive that metformin might be effective in treating rat fatty liver induced by high fat feeding.

Animals↗
PubMed1998

Association of fatty liver with increased ratio of visceral to subcutaneous adipose tissue in obese men.

We studied the association of fatty liver with subcutaneous and visceral obesity in 46 male and 36 female patients with body mass index (BMI) over 22 kg/m2. The correlation coefficient between the ratio of the visceral adipose tissue to the subcutaneous adipose tissue (V/S) and the computed tomography (CT) number of the liver was -0.299 (P < 0.05) and that between the V/S ratio and the ratio of the CT number of the liver to that of the spleen (CT-L/CT-S) was -0.335 (P < 0.05) in the males. Partial correlation analysis after making correction for BMI showed an increased correlation coefficient of -0.485 (P < 0.05) between the V/S ratio and the CT-L/CT-S ratio in the males. The odds ratio in the males for CT-L/CT-S below 1.0 and V/S above 1.0 was 3.25 with a 95% confidence interval of 1.02 to 9.39. No such association between the V/S ratio and the CT-L/CT-S ratio was present in the female patients. Multiple regression analysis with serum level of alanine aminotransferase, a marker of fatty liver, as an independent variable revealed a partial regression coefficient of -17.7 for CT-L/CT-S (P < 0.05) in the males and -21.7 (P < 0.05) in the females, validating the CT-L/CT-S ratio as an index of fatty liver. The results indicate the association of fatty liver as determined by the CT-L/CT-S ratio with visceral obesity in males.

Adipose Tissue↗
PubMed2006

Research on the protection effect of pioglitazone for non-alcoholic fatty liver disease (NAFLD) in rats.

OBJECTIVE: The prevalence of non-alcoholic fatty liver disease (NAFLD) has markedly increased. Insulin resistance has been implicated in the pathogenesis of NAFLD. This study was aimed at observing the relationship between insulin resistance and NAFLD, and evaluating the role of pioglitazone (PGZ) acting as insulin-sensitizing agents in the prevention and treatment of rat fatty liver induced by high fat feeding. METHODS: The rats were separated randomly into 6 groups: model group I were fed high fat diet for 8 weeks, PGZ prevention group were given PGZ 4 mg/(kg.d) simultaneously, while control group I were fed normal food for 8 weeks; model group II were fed high fat diet for 16 weeks, PGZ treatment group were given PGZ 4 mg/(kg.d) orally simultaneous with high fat diet for 8 weeks after high fat feeding for 8 weeks, control group II were fed normal food for 16 weeks. The rats were sacrificed after 8 weeks and 16 weeks respectively. Liver weight, body weight, serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), tumor necrosis factor alpha (TNF-alpha), fasting blood glucose (FBG), fasting plasma insulin (FINS), HOMA (homeostasis model assessment) insulin resistance index (HOMA-IR), and the liver histology of rats of all groups were assayed. RESULTS: After 8 weeks, the liver in model group I showed typical steatosis, accompanied with mild to moderate lobular inflammatory cell infiltration, liver indexes and serum levels of ALT, AST, ALP, TNF-alpha were significantly increased (P<0.05) compared with control group I. Whereas, the degree of hepatic injury was attenuated in PGZ prevention group, liver indexes and serum levels of ALT, ALP were significantly decreased (P<0.05) compared with model group I. After 16 weeks, notable steatosis, and lobular inflammation were observed in model group II rat liver, while the degree of hepatic injury was attenuated in the PGZ treatment group. Liver index, serum levels of ALT, AST, ALP, FINS and HOMA-IR were significantly increased (P<0.05) in model group II compared with control group II. Whereas, in PGZ treatment group, serum levels of AST and FINS showed decreasing tendency, liver indexes, serum levels of ALT, ALP, TNF-alpha and HOMA-IR were significantly decreased compared with model group II. CONCLUSION: Insulin resistance plays a role in the pathogenesis of NAFLD in rats. Pioglitazone can attenuate insulin resistance and biochemical and histological injury in high fat-induced fatty liver in rats.

Alanine Transaminase↗
PubMed2004

Identification of novel molecular candidates for fatty liver in the hyperlipidemic mouse model, HcB19.

The inbred HcB19 mouse strain expresses a truncated form of thioredoxin interacting protein and is phenotypically characterized by fatty liver and elevated plasma triglycerides and VLDL. Recently, these mice have been proposed as an animal model for familial combined hyperlipidemia. The aim of the present study was identification of hepatic proteins specifically associated with the presence of fatty liver. Eighteen differential proteins were detected in whole-liver homogenate from HcB19, or the parental strain C3H, using 2D electrophoresis, and 11 of those were successfully identified by mass spectrometry. Five of the identified differential proteins were mitochondrial, two peroxisomal, two cytosolic, and two secretory. Four differential proteins were novel in the fatty liver proteome [i.e., aconitase, succinate dehydrogenase, propionyl CoA carboxylase alpha chain (PCCA), and 3-hydroxyanthranilate 3,4 dioxygenase (3HAAO)]. Of these, PCCA and 3HAAO are of particular interest because of their known functions in nicotinic acid metabolism (3HAAO) and ketogenesis (PCCA). We have newly identified several differential proteins in the hepatic proteome of mice with fatty liver, including PCCA and 3HAAO, and confirmed differential expression of previously reported proteins. These individual proteins, PCCA and 3HAAO, can be important in development of fatty liver or in the expression of hyperlipidemia.

Animals↗
PubMedDate not supplied

S-adenosylmethionine generation and prevention of alcoholic fatty liver by betaine.

Earlier studies by other investigators have shown that S-adenosylmethionine (SAM) has the capacity to attenuate liver injury in experimental animals. In a recent study in this laboratory, it was shown that when supplemental dietary betaine was given to control and ethanol-fed rats at the level of 0.50% (W/V), SAM levels were doubled in the livers of control animals and increased fivefold in livers of ethanol-fed rats. The increased levels of SAM in the livers of ethanol-fed animals protected the livers from fatty infiltration due to ethanol feeding. In this study, an attempt was made to determine the minimum level of dietary betaine that protects against the fatty infiltration. Levels of betaine at 0.05%, 0.10%, 0.25%, and 0.50% in semiliquid control and alcohol diets were tested in rats for 30 days. When hepatic betaine, SAM, and triglyceride levels were determined, it was demonstrated that only the dietary level of betaine at 0.50% supplied enough hepatic betaine to generate the level of SAM that was required to protect against the alcoholic steatosis resulting from the dietary ethanol. These results suggest that betaine, when given in sufficient amounts, may be a promising therapeutic agent in the treatment of liver disease.

Animals↗
PubMed1994

Unsaturated fat and low energy intake induce whereas an increment in energy intake ameliorates fatty liver during prolonged alcohol consumption by rats.

Two groups of rats were fed liquid diets containing 35% of energy as fat and either 36 or 26% of energy as alcohol to examine the effect of fat and energy intake on alcoholic fatty liver production. After 4 wk, five rats in each group were killed for analysis of liver triglyceride concentration, and then the alcohol diets fed to remaining rats were switched. All remaining rats were killed for hepatic triglyceride determination after another 4 wk. Rats initially fed the 36% alcohol diet or those switched to this diet ingested less energy, exhibited alcoholemia and slow growth, and developed fatty livers. Rats initially fed the 26% alcohol diet or those switched to this diet ingested significantly more energy, high amounts of alcohol and fat, exhibited low alcoholemia and faster growth than when they were fed the 36% alcohol diet. Fatty liver was absent in rats fed the 26% alcohol diet but was induced when they were fed the 36% alcohol diet. Fatty liver in rats initially fed the 36% alcohol diet regressed completely when the rats were switched to the 26% alcohol diet. Additional studies employing 36% alcohol diets containing 35% of energy as fat, derived from either corn oil or olive oil, revealed that unsaturated fat and not specifically linoleate plays a role in the induction of fatty liver. Thus, nutritional factors regulate the induction or regression of fatty liver and alcoholemia in alcoholic rats.

Alcoholism↗