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PubMed1976

An association of hardness of water with incidence of fatty liver syndrome in laying hens.

Twenty-one samples of water were collected from commercial egg production farms in Georgial with or without a history of fatty liver syndrome. These samples plus a sample of water from the University of Georgia Poultry Farm were analyzed for various mineral elements by atomic absorption, direct reading emission spectroscopy and by neutron activation. Water samples from farms with a history of fatty liver syndrome had signficantly more calcium, magnesium, strontium, sodium, iron and barium than water samples from farms reporting no significant problem with fatty liver syndrome. Levels of manganese, boron, copper zinic and aluminum were not significantly different. Although the results do not prove that water quality is the cause of the disease, they do demonstrate an association of hardness of water with fatty liver syndrome that should be further investigated.

Animals↗
PubMed2002

Other disease associations with non-alcoholic fatty liver disease (NAFLD).

Non-alcoholic fatty liver disease (NAFLD) is usually seen in middle-aged women with obesity, non-insulin-dependent diabetes mellitus and/or hyperlipidaemia. NAFLD has also been associated with other conditions. Surgical procedures to treat obesity such as jejunoileal bypass and gastroplasty as well as massive small bowel resection have been associated with NAFLD. Mechanisms such as rapid weight loss, certain nutritional deficiencies and bacterial overgrowth have been proposed. Other nutritional conditions such as extreme malnutrition and total parenteral nutrition can also cause NASH. This can be due to abnormal glucose and fat metabolism, deficiencies like carnitine, essential fatty acid and choline or, in the case of parenteral nutrition, excess of calories, glucose or lipids. Several drugs have also been implicated as well as some inborn errors of metabolism and, more rarely, other diseases.

Digestive System Surgical Procedures↗
PubMed1979

Serum and body characteristics of laying hens with fatty liver syndrome.

Commercial laying hens with Fatty Liver Syndrome had greatly elevated levels of serum calcium and cholesterol. Most of the hens with the elevated serum calcium and cholesterol were out of production, but some were still in production. Hens with elevated calcium and cholesterol levels had extremely large combs and excessive deposits of fat in the abdomen.

Adipose Tissue↗
PubMed2005

Nonalcoholic fatty liver disease: a clinical review.

Nonalcoholic fatty liver disease may be the most common liver disease in the United States, with a high prevalence in the obese, type 2 diabetic population, and it is probably underestimated as a cause for cirrhosis. Clinicopathologically, it represents a wide spectrum of histologic abnormalities and clinical outcomes, ranging from benign hepatic steatosis to cirrhosis. Pathophysiologically, insulin resistance is thought to be pivotal in the development of steatosis, after which a second oxidative stressor produces lipid peroxidation and nonalcoholic steatohepatitis (NASH). Liver biopsy is the gold standard for diagnosis and prognosis. The need for an effective treatment is both clear and urgent, yet in the absence of proven therapies, treatment is directed toward weight loss and comorbidity management. For patients with NAFLD at risk of disease progression, there is a lack of large, randomized, placebo-controlled trials of adequate treatment duration, with baseline stratification according to histologic severity.

Fatty Liver↗
PubMed2004

Nonalcoholic fatty liver disease and nonalcoholic steatohepatitis.

Nonalcoholic fatty liver disease (NAFLD) is a well-recognized form of chronic liver disease affecting both children and adults that has gained increased recognition. Recently NAFLD has been associated with insulin resistance and its incidence and prevalence is likely increasing, paralleling the rise in obesity and diabetes mellitus in the United States. The article includes current thoughts on the natural history and pathogenesis of NAFLD and describes current trends in the diagnosis and treatment of this condition.

Chronic Disease↗
PubMed2006

The Fatty Liver Index: a simple and accurate predictor of hepatic steatosis in the general population.

BACKGROUND: Fatty liver (FL) is the most frequent liver disease in Western countries. We used data from the Dionysos Nutrition & Liver Study to develop a simple algorithm for the prediction of FL in the general population. METHODS: 216 subjects with and 280 without suspected liver disease were studied. FL was diagnosed by ultrasonography and alcohol intake was assessed using a 7-day diary. Bootstrapped stepwise logistic regression was used to identify potential predictors of FL among 13 variables of interest [gender, age, ethanol intake, alanine transaminase, aspartate transaminase, gamma-glutamyl-transferase (GGT), body mass index (BMI), waist circumference, sum of 4 skinfolds, glucose, insulin, triglycerides, and cholesterol]. Potential predictors were entered into stepwise logistic regression models with the aim of obtaining the most simple and accurate algorithm for the prediction of FL. RESULTS: An algorithm based on BMI, waist circumference, triglycerides and GGT had an accuracy of 0.84 (95%CI 0.81-0.87) in detecting FL. We used this algorithm to develop the "fatty liver index" (FLI), which varies between 0 and 100. A FLI < 30 (negative likelihood ratio = 0.2) rules out and a FLI > or = 60 (positive likelihood ratio = 4.3) rules in fatty liver. CONCLUSION: FLI is simple to obtain and may help physicians select subjects for liver ultrasonography and intensified lifestyle counseling, and researchers to select patients for epidemiologic studies. Validation of FLI in external populations is needed before it can be employed for these purposes.

Adult↗
PubMed2004

High prevalence of metabolic complications in patients with non-alcoholic fatty liver disease.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is considered to be the liver component of the metabolic syndrome and is frequently associated with obesity, dyslipidemia and type II diabetes mellitus (NIDDM). We aimed to determine the development of liver function tests (LFTs) and metabolic complications in patients previously diagnosed with NAFLD. METHODS: One-hundred-and-two patients with NAFLD diagnosed in the period 1994-2001 were identified. Eighty were brought in for new investigations, including LFTs, blood pressure, BMI, lipid profile, blood glucose and insulin. Original liver biopsy was re-evaluated. RESULTS: Sixty-two patients (77%) were males (median age 46 years; mean follow-up time 2.8 +/- 1.2 years). Fifty-four patients (68%) were light to moderately overweight with body mass index (BMI) 25-30 kg/m. Mean BMI (28.2) was the same at diagnosis and at follow-up (28.3). At the new examination, 18 patients (23%) had developed diabetes mellitus type II (n = 6) or had impaired fasting glucose (IFG) (n = 12), compared to only 2 patients at diagnosis. Hyperinsulinemia was observed in 19 patients (24%). Dyslipidemia, with elevated triglycerides and/or hypercholesterolemia, was now present in 65 patients (81%). Twenty-two patients (27%) had hypertension compared to 9 (11%) at diagnosis. Liver biopsy was performed in 24%, and 89% of those fulfilled the criteria for NASH. However, mild inflammation and fibrosis was observed, grade 1-2 (n = 17), stage I-II (n = 13) and none had cirrhosis. CONCLUSION: A significant proportion of patients with both clinical and histological diagnosis of NAFLD develop metabolic problems soon after diagnosis. These patients should be screened regularly for metabolic disorders.

Adult↗
PubMed2000

[Effects of pravastatin on hepatic plasminogen activator inhibitor 1 mRNA expression in rabbits with fatty liver].

OBJECTIVE: To explore the effects of Pravastatin on the changes of plasminogen activator inhibitor 1 (PAI-1) gene expression of hepatic tissue in rabbit with fatty liver. METHODS: We observed the influences of Pravastatin on the rabbit model of hyperlipidemia and fatty liver induced by high fat diet for 12 weeks, and the plasma PAI-1 activity and the hepatic PAI-1 mRNA expression in therapeutic group (n=10); and meanwhile, designed the model group (n=10) and normal group (n=7) as control. RESULTS: Severe hepatocellular steatosis was found in model group compared with normal group. Plasma lipids and PAI-1 activity increased in model group in 6 and 12 weeks, and was significantly higher than normal group in 12 weeks. PAI-1 mRNA relative values in hepatic tissue in model group were higher than those in normal group. Compared with model group, hepatic pathological manifestation with the respect of steatosis had no obvious changes in therapeutic group, but the lipid content and PAI-1 activity in the plasma and the expression of PAI-1 mRNA in the liver were significantly reduced. The activity of PAI was (14.0A2. 5)X10(-3)U/L in model group, and (8.6A2.0)X10(-3)U/L in therapeutic group in 12 weeks. CONCLUSION: Pravastatin could inhibit over-expression of PAI-1 mRNA in the rabbit liver with hyperlipidemia and fatty liver, and reduce its plasma PAI-1 activity.

Animals↗
PubMed2004

Non-alcoholic fatty liver disease, non-alcoholic steatohepatitis and orthotopic liver transplantation.

Obesity, non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are becoming increasingly common medical problems in the developed world, often in the setting of the metabolic or insulin resistance syndrome (IRS). It is predicted that by the year 2025 > 25 million Americans may have NASH-related liver disease. NASH and NAFLD also affect the donor population. The use of steatotic donor livers for liver transplantation (LT) is associated with an increased risk of primary nonfunction (PNF) in the allograft. There is particular reluctance to use steatotic livers for living donor LT. There is indirect evidence to suggest that patients undergoing LT for cirrhosis resulting from NASH may have poorer outcome, despite careful selection of LT candidates. Indeed it is likely that many potential LT candidates with NASH are excluded from LT due to co-morbid conditions related to IRS. The post-LT patient is at risk of several components of IRS, such as diabetes mellitus, hypertension, hyperlipidaemia and obesity and there is increasing recognition of de novo and recurrent NAFLD and NASH after LT. Thus NAFLD and NASH affect all aspects of LT including donors, patients in evaluation and the LT recipient.

Fatty Liver↗
PubMed1975

Carbohydrate absorption by chicks affected with the fatty liver and kidney syndrome.

Chicks with fatty liver and kidney syndrome (FLKS) were given oral doses of one of the following test solutions: water, glucose, maltose, starch. Plasma glucose concentration was measured during the four subsequent hours. All FLKS-affected chicks were hypoglycaemic before treatment. Although in some cases plasma glucose concentration increased slightly in the FLSK-chicks given water alone, significantly greater increases were invariably observed following the administration of carbohydrate to sick birds. Results obtained from dietary experiments in which starch was replaced by glucose in a ration causing high mortality from the syndrome revealed no beneficial effect due to the substitution. It was concluded that FLKS does not involve any major impairmant of carbohydrate digestion or absorption.

Animals↗
PubMed2003

Serum leptin level can be a negative marker of hepatocyte damage in nonalcoholic fatty liver.

BACKGROUND: The aim of this study was to determine whether leptin and insulin resistance (IR) showed differences between steatotic patients with and without elevated serum transaminases. METHODS: The study included 32 patients with fatty liver and high serum transaminase level (group I), 31 patients with fatty liver and normal serum transaminase level (group II), and 8 nonobese and nonsteatotic controls. The presence of steatosis was demonstrated by ultrasonography. Due to the effect of body mass index (BMI) on leptin levels, groups I and II were divided to form four subgroups for analysis (group IA, BMI 30; group IIA, BMI 30. RESULTS: The serum leptin levels in group IIB were significantly higher than the levels in group IB ( P = 0.017). Serum leptin was also higher in group IIA than in group IA, but this difference was not statistically significant ( P = 0.097). Logistic regression analysis revealed a significant negative correlation between serum leptin level and the presence of a high transaminase level (odds ratio, 0.97; 95% confidence interval, 0.95-0.99). The levels of IR in the four patient groups were comparable, but the controls had significantly lower IR levels than group IIA. CONCLUSIONS: Elevated serum leptin seems to be a feature of steatotic patients with normal transaminase levels, and the level of serum leptin seems to decrease as the hepatocyte injury develops. IR is a common feature of fatty liver disease, irrespective of the presence of hepatocellular necrosis.

Adult↗
PubMed2006

Hyaluronic acid levels can predict severe fibrosis and platelet counts can predict cirrhosis in patients with nonalcoholic fatty liver disease.

BACKGROUND AND AIM: Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of liver disease from simple steatosis to cirrhosis. Therefore, markers for predicting NAFLD with advanced fibrosis are needed. The aim of this study was to establish non-invasive predictive markers of liver fibrosis in NAFLD. METHODS: One hundred and forty-eight patients were diagnosed as having biopsy-proven NAFLD. In order to separately identify severe fibrosis (bridging fibrosis plus cirrhosis) and cirrhosis, the patients were analyzed twice: first, as mild fibrosis versus severe fibrosis; and second, as non-cirrhosis versus cirrhosis. Univariate and multivariate analyses were conducted. The diagnostic ability to detect severe fibrosis and cirrhosis was assessed by the area under the receiver operating characteristic curve. The cut-off values of serum markers to detect severe fibrosis and cirrhosis were determined. RESULTS: Hyaluronic acid was selected as a predictive marker for severe fibrosis. A cut-off value of 42 ng/mL of hyaluronic acid had a 100% predictive value for patients free of severe fibrosis and was associated with an optimal combination of sensitivity (100%, 95% confidence interval [CI] 90-100%) and specificity (89%, 95%CI 80-94%). The platelet count was found to be an independent predictor of cirrhosis. A cut-off value of 16 x 10(4)/microL for the platelet count was associated with an optimal combination of sensitivity (100%, 95%CI 82-100%) and specificity (95%, 95%CI 90-98%). CONCLUSIONS: Hyaluronic acid levels can accurately identify NAFLD patients with severe fibrosis, and the platelet count can identify NAFLD patients with cirrhosis. Thus, these markers offer a good guideline for the assessment of hepatic fibrosis in the many patients with NAFLD.

Adolescent↗
PubMedDate not supplied

Enalapril prevents fatty liver in nephrotic rats.

BACKGROUND: A number of clinical entities, including nephrotic syndrome, present light to moderate enlargement of the liver due to accumulation of neutral fats (triglycerides) in the hepatocytes. Even though the outcome of hepatic steatosis does not seem to be harmful, when an additional inflammatory component is present, a variable degree of hepatic fibrosis and chronic liver disease could occur. In the last few years, ACE inhibitors have demonstrated multifunctional properties beyond their hemodynamic effects, especially as anti-inflammatory modulators and anti-oxidative stress agents. The purpose of the present study was to evaluate the possible protective action of an ACE inhibitor, enalapril (E), on fatty liver in adriamicyn-induced nephrotic rats (NR). METHODS: Two-month-old male Sprague-Dawley rats were separated into four groups. Control Group (G1, n = 18), N Group (G2, n = 18); NR + E Group (G3, n = 18), E Group (G4, n = 18). To induce an experimental model of nephrot ic syndrome, G2 and G3 received a single injection of adriamycin (7.5mg/kg b.w.) I.V. For twelve weeks, G3 and G4 received E daily at a concentration of 20 mg/L in their drinking water. At the end of the study, liver lesions were evaluated using standard staining. In order to detect fat in the liver and identify activated hepatic stellate cells (HSCs), inflammatory cell infiltration and amount of hepatic TGFI1, Oil red O and monoclonal antibodies (anti-a-smooth muscle actin, anti-monocytes/macrophages and anti-TGFbeta1) were used respectively. Hepatic lesions were quantified by semiquantitative scores. Creatinine clearance, urinary albumin excretion, serum lipids and liver enzymes were also studied to evaluate renal and liver function. RESULTS: Although having the same serum lipid levels, G3 rats (NR + E) when compared with the nephrotic rats of G2 showed: 1) fewer liver lesions: a) fatty liver (% hepatocytes with fatty deposits): 36.6 +/- 11.4 vs. 4.2 +/- 4.9; p < 0.01; b) hepatic necrosis score: 1.22 +/- 0.42 vs. 0.13 +/- 0.28; p< 0.01; c) ED1 (monocytes/macrophages) score: 1.33 +/- 0.48 vs. 0.30 +/- 0.30; p < 0.01; d) HSCs score: 1.02 +/- 0.26 vs. 0.08 +/- 0.19; p < 0.01; e) liver interstitial TGFbeta1 score 0.75 +/- 0.5 vs. 0.08 +/- 0.19; p < 0.01; p < 0.01; f) liver fibrosis score: 1.11 +/- 0.32 vs. 0.08 +/- 0.19; p < 0.01; 2) lower serum liver enzymes: a) SGOT: 581.7 +/- 91.1 UI/L vs. 303.3 +/- 46.2 UI/L; p < 0.05; b) SGPT: 170.7 +/- 31.1 UI/L vs. 81 +/- 15.8 U.I./L; p < 0.05. Rats from G2 (NR) showed a positive and significant correlation between serum cholesterol and serum triglycerides and % fatty liver (r = 0.72 p 0.01 and r = 0.77 p < 0.01 respectively). This relation was not found in animals in G3 (NR+E). CONCLUSIONS: In the present study enalapril showed a significant protective effect on hepatic steatosis and its inflammatory reaction. These data suggest that enalapril treatment in nephrotic syndrome, beyond its specific antiproteinuric and renoprotective effects, could provide additional liver protection.

Administration, Oral↗
PubMed2004

The epidemiology of fatty liver.

There are insufficient data available on the epidemiology of fatty liver to design a complete and correct view of the prevalence, incidence and natural history of this disorder. This article, mainly based on the revision of recently published papers in this field, attempts to give an overview of the current findings on the epidemiology of fatty liver worldwide. The possible factors involved in the development of fat accumulation in the liver, and their potential role in the progression of the disorder will be also addressed.

Alcoholism↗
PubMed2005

Should nonalcoholic fatty liver disease be renamed?

BACKGROUND: None of the synonyms of nonalcoholic fatty liver disease (NAFLD) include clinical correlates nor do they mention insulin resistance, a recognized determinant of the etiopathogenesis and natural history of NAFLD. METHOD: The literature concerning the pathogenesis and definition of NAFLD is reviewed. RESULTS: The reasons why NAFLD should be renamed are: (a) clinically meaningful hepatic steatosis could be present at less than 5% triglyceride hepatic content; (b) steatosis is usually no longer observed in the most advanced forms of NAFLD ('cryptogenic cirrhosis'); (c) the concurrence of metabolic derangements could be more important than alcohol in the pathogenesis of alcoholic liver disease; (d) a concurrent metabolic etiology might worsen the course of chronic HCV and autoimmune hepatitis; (e) in NAFLD the liver is a target organ of the metabolic syndrome, a systemic subclinical inflammatory state. CONCLUSION: The introduction of a positive criterion also mentioned in its definition would benefit the diagnosis of NAFLD and of steatohepatitis observed in the setting of other liver diseases, help to estimate the risk of its progression and aid the treatment of metabolic (fatty) liver disorders. There is a compelling need for an experts' agreement on a new definition of insulin resistance/metabolic-related liver disease.

Chronic Disease↗
PubMed1994

Ammonium chloride inhibits pyruvate oxidation in rat liver mitochondria: a possible cause of fatty liver in Reye's syndrome and urea cycle defects.

1. Earlier studies with liver slices showed that inhibition by NH4+ of the oxidation of palmitate to CO2 was greater than total oxidation, whereas salicylate exerted a stronger inhibitory effect on the latter. We have now investigated the effects of NH4Cl and salicylate on ADP-induced O2 consumption by mitochondria (State 3 rate) respiring on pyruvate, and oxidation of [1-14C]- and [2-14C]-pyruvate to 14CO2. 2. The rate of State 3 respiration was inhibited and plateaued at 45% with 10 mmol/l NH4Cl. 3. Oxidation of [1-14C]pyruvate was not significantly affected by either NH4Cl or salicylate. Oxidation of [2-14C]pyruvate was strongly inhibited and plateaued at 70% with 1 mmol/l NH4Cl (IC50 = 0.125 mmol/l). ADP (1 mmol/l) increased the rate of decarboxylation of [2-14C]pyruvate but the extent of NH4Cl inhibition was not affected. Salicylate had a slight activating effect in the absence or presence of NH4Cl. 4. These results indicate that NH4Cl inhibits the oxidative metabolism of acetyl-CoA in the tricarboxylic acid cycle. Therefore, inhibition of fatty acid oxidation to acetyl-CoA as well as its further oxidative metabolism occurring under hyperammonaemia (> 0.1 mmol-1.49 mmol/l in Reye's syndrome patients) may be one of the causes of fatty acidaemia. 5. The cumulative inhibitory effects of NH4+ and fatty acyl derivatives on mitochondrial oxidative metabolism and production of ATP, as well as the uncoupling effects of salicylate, may contribute to some of the pathophysiology observed in patients with Reye's syndrome, and enzyme defects of the urea cycle.

Adenosine Diphosphate↗
PubMed1995

Induction of HSP72 in rat liver by chronic ethanol consumption combined with exercise: association with the prevention of ethanol-induced fatty liver by exercise.

Ethanol-induced fatty liver in rats was attenuated by repeated running exercise, and the protective effect of exercise was associated with the synergistic expression of heat shock proteins (HSP72). Rats were placed in four groups of six. The two ethanol-fed groups of rats received a liquid diet (Lieber-DeCarli formulation) in which 36% of the calories were derived from ethanol. One group remained sedentary (S/E), whereas the other was trained to run on a rodent treadmill at a speed of 27 m/min, 1 hr/day, 5 days/week, for 7 weeks (R/E). Two other groups--one exercised as previously mentioned (R/C) and one sedentary (S/C)--received control-liquid diets in which the ethanol was isocalorically substituted with a dextran/maltose mixture. The degree of fatty infiltration in liver sections stained with hematoxylin and eosin was graded on a 0-4 scale and the data analyzed by ANOVA on ranks. Ethanol significantly induced fatty infiltration in the S/E group, whereas fatty infiltration in the livers of the R/E group was not different from the S/C group. Electrophoresis and Western blotting of liver homogenates demonstrated that HSP72 was not expressed in either the S/C or S/E groups and was only slightly expressed in the R/C group. The combination of exercise and ethanol, however, resulted in an elevated expression of HSP72 in the R/E group. The content of HSP73 was unaffected by any treatment.

Animals↗
PubMed2002

Size and oxidative susceptibility of low-density lipoprotein particles in breast cancer patients with tamoxifen-induced fatty liver.

The purpose of the present study was to investigate the effects of tamoxifen on the size and oxidative susceptibility of low-density lipoprotein (LDL) particles in breast cancer patients with tamoxifen-induced fatty liver. We investigated the following breast cancer patients: 13 receiving no tamoxifen (group A), 13 receiving tamoxifen 40 mg daily but without fatty liver (group B), and 13 receiving tamoxifen 40 mg daily with fatty liver (group C). Plasma lipids and diameter of LDL particles were measured. Susceptibility of LDL to oxidation was analyzed by incubation with CuSO(4) while monitoring conjugated diene formation and assaying thiobarbituric acid reactive substances (TBARS). Plasma total and LDL cholesterol concentrations in groups B and C were significantly lower than those in group A. In group C, concentrations of plasma triglyceride (TG) and TBARS were significantly greater, but LDL particle diameter and lag time for LDL oxidation were significantly smaller than those in groups A and B. Plasma TG concentrations correlated negatively with computed tomography ratio of liver to spleen (r = -0.76; P < 0.001). LDL particle diameter correlated negatively with plasma TG (r = -0.62; P < 0.001) and TBARS (r = -0.44; P < 0.01), but positively with LDL lag time (r = 0.47; P < 0.01). Tamoxifen-induced fatty liver in breast cancer patients may be atherogenic, via increased TG and consequent small, easily oxidized LDL particles.

Adult↗