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PubMed2001

Treatment of nonalcoholic fatty liver: present and emerging therapies.

Treatment of patients with nonalcoholic fatty liver has typically been focused on the management of associated conditions such as obesity, diabetes mellitus, and hyperlipidemia as well as discontinuation of potentially hepatotoxic drugs. Nonalcoholic fatty liver associated with obesity may resolve with weight reduction, although the benefits of weight loss have been inconsistent. Appropriate metabolic control for patients with diabetes mellitus or hyperlipidemia is always recommended but not always effective in reversing nonalcoholic fatty liver. Promising results of pilot studies evaluating ursodeoxycholic acid, gemfibrozil, betaine, N-acetylcysteine, and alpha-tocopherol suggest that these medications may be of potential benefit in the treatment of patients with nonalcoholic fatty liver. These medications, however, need first to be tested in well-controlled trials with clinically relevant end points and extended follow-up. A better understanding of the pathogenesis and natural history of this condition will help to identify the subset of patients with nonalcoholic fatty liver at risk of progressing to advanced liver disease and, hence, the subgroup of patients who should derive the most benefit from medical therapy. In this article, we review (1) the existing medical therapy for patients with nonalcoholic fatty liver, (2) the emerging data from clinical trials evaluating potentially useful medications, and (3) the potential therapeutic implications of recent studies on the pathogenesis of this liver disease.

Diabetes Mellitus, Type 2↗

PubMed2004

[Associated risk factors of fatty liver in the patients with type 2 diabetes mellitus].

OBJECTIVE: To analyze the associated risk factors, clinical characteristics and laboratory abnormalities of type 2 diabetes patients with fatty liver. METHODS: The data of type 2 diabetes cases with fatty liver were collected in our hospital. 63 cases of type 2 diabetes without fatty liver were selected randomly as control during the same period. The associated variables were analyzed by using logistic regression model. The clinical data and liver function were compared between two groups. RESULTS: The proportion of obesity and hyperlipidemia was higher in type 2 diabetes patients with fatty liver than without fatty liver. Body mass index (BMI) (OR: 4.392) was positive correlation to fatty liver in the patients with type 2 diabetes. In contrast, insulin sensitivity index (ISI) (OR: 0.000) and regular insulin treatment (OR: 0.058) were negative correlation to it. The abnormal frequencies of aspartate aminotransferase (AST, 16.0%), alanine aminotransferase (ALT, 25.2%), the ratio of AST/ALT less than 1 (52.8%) and gamma-glutamyltransferase (GGT, 31.9%) of type 2 diabetes patients with fatty liver were significantly higher than those without fatty liver (3.2%, 6.4%, 36.5% and 11.1% respectively). CONCLUSION: Obesity and insulin resistance might increase the risk of fatty liver in the patients with type 2 diabetes. Patients of type 2 diabetes with fatty liver show higher serum lipid level and more obvious damages of liver function than those without fatty liver

Adult↗

PubMed1983

A case of idiopathic fatty liver detectable only by ultrasonography.

A 40-year-old man was diagnosed as fatty liver according to our ultrasonographical criteria for fatty liver, i.e., liver-kidney contrast in the ultrasound mass screening of the liver, biliary tract and pancreas. He lacked any signs or symptoms, nor any known causes of fatty liver, i.e., obesity, diabetes, hyperlipidemia, ingestion of alcohol or drugs. Liver biopsy of this patient revealed fatty change of about 50% of the hepatic lobules. It has been difficult to suspect the presence of latent fatty liver which lacked both the abnormality in the liver function test and hepatomegaly, and even impossible when it lacked any risk factors. In the future as the ultrasonography becomes more generally used as a primary screening examination, "idiopathic latent fatty liver", like this patient, will be more frequently found and this, in turn, will contribute to the progress of the epidemiology and etiology of fatty liver.

Adult↗

PubMed2005

Roux-en-Y gastric bypass improves liver histology in patients with non-alcoholic fatty liver disease.

OBJECTIVES: Non-alcoholic fatty liver disease (NAFLD) is the most common cause of liver disease in the United States and is prevalent in morbidly obese patients. While weight loss and treatment of risk factors are recommended, the reported effects of bariatric surgery on NAFLD are mixed. RESEARCH METHODS AND PROCEDURES: We examined liver histology at the time of Roux-en-Y gastric bypass surgery and at elective incisional hernia repair after weight loss for 16 patients at one center. Slides were read by one pathologist, blinded to clinical data, using the Brunt criteria. Clinical and laboratory data were extracted from chart review. Alcohol use was ascertained by two interviews. RESULTS: At baseline, the mean age was 44 years, 50% were women, 88% were white, and the mean BMI was 51 kg/m2. None had significant alcohol use. On initial biopsy, all patients showed steatosis, 94% had inflammation, 88% had ballooning degeneration, 88% had perisinusoidal fibrosis, and 81% had portal fibrosis. The mean time between the two biopsies was 305 +/- 131 (SD) days. The mean weight loss was 118 +/- 29 lb. Steatosis improved in 15 of 16 patients, with resolution in 13. Twelve of 15 patients with inflammation at baseline showed improvement, and 12 of 14 showed less ballooning. Six of 14 patients with perisinusoidal fibrosis and 6 of 13 with portal fibrosis showed improvement. No patient had worsening of steatosis, inflammation, ballooning, or fibrosis. DISCUSSION: Our study shows improvement in all of the histological features of NAFLD after Roux-en-Y gastric bypass surgery-induced weight loss, despite significant histopathology at baseline and substantial weight loss.

Adult↗

PubMed2004

Role of free radicals in failure of fatty liver grafts caused by ethanol.

Alcohol is associated with accidental deaths and suicides leading to organ donation, and hepatic steatosis is an important risk factor for initial poor function and failure of human liver grafts. Mechanisms of fatty graft failure are not fully understood, but increased oxidative stress may be a major factor. To characterize the role of free radical stress and the efficacy of antioxidant treatments in fatty liver graft injury, donors for orthotopic rat liver transplantation were treated chronically (3 or more weeks) and acutely (single dose) with ethanol. After transplantation, necrosis and alanine aminotransferase release were threefold to fourfold higher in recipients of fatty grafts from donors treated with ethanol either acutely or chronically compared with findings for recipients of grafts from untreated donors. Moreover, graft survival decreased from nearly 100% to less than 20%. Free radical adducts, as measured by electron spin resonance spectroscopy, were detected in the blood and bile of rats receiving fatty grafts caused by ethanol. Markers of lipid peroxidation also increased after transplantation. Destruction of Kupffer cells with gadolinium chloride decreased free radical production and improved graft survival. Leukocyte adhesion increased beginning early after implantation, and adherent white blood cells obtained from transplanted fatty livers produced the same free radical species as were detected in blood. Therefore, Kupffer cells and adherent white blood cells are important sources of free radicals. Free radicals not only damage fatty grafts directly but also lead to enhanced inflammation and disturbed microcirculation. Delivery of superoxide dismutase-1 and superoxide dismutase-2 genes, free radical-scavenging polyphenols, and antioxidant-containing Carolina Rinse solution reduced injury and improved survival of fatty grafts caused by ethanol. Taken together, these findings indicate that free radicals increase in fatty grafts after transplantation and play an important role in injury of fatty grafts obtained from ethanol-exposed donors. Treatment of fatty donor livers with antioxidants and free radical scavengers may thus be an effective clinical therapy to prevent failure of fatty grafts.

Animals↗

PubMed1988

Plasma lipoproteins and fatty liver in dairy cows.

Dairy cows were classified on the basis of a histological study after a hepatic biopsy conducted in the second week post partum (mild fatty liver, moderate fatty liver, severe fatty liver). Plasma lipoproteins were separated into various density classes by repeated ultracentrifugation. The results indicate that the beginning of lactation is associated with a low concentration of the 1.006 to 1.063 g ml-1 lipoprotein fraction. The lowest concentrations occurred in cows with severe steatosis or during the evolution of moderate steatosis.

Animals↗

PubMed2001

Perioperative care of a patient with acute fatty liver of pregnancy.

Acute fatty liver of pregnancy (AFLP) is a late gestational complication with biochemical similarities to the inherited disorders of mitochondrial fatty acid oxidation and clinical similarities to fulminant hepatic failure. The following case illustrates our perioperative management of this rarely encountered disorder.

Acute Disease↗

PubMed1990

Prediction of fatty liver from serum triglyceride levels and body weight indexes.

Fatty liver is a common disease in Taiwan. In this study, we tried to evaluate the validity of predicting the presence of fatty liver from clinical data instead of liver biopsy or sonography. From a community survey in Putai, a total of 873 adults older than 30 years and quantified as to triglyceride level, body height, body weight, and the results of the oral glucose tolerance test and upper abdominal sonography were recruited for analysis. Using a receiver operating characteristic (ROC) curve, the best 'cutoff values' for determination of fatty liver were predicted from body weight index and serum triglyceride level in 8 clusters grouped by sex, age and presence or absence of diabetes mellitus. The best cutoff values of triglyceride in the 8 clusters varied from 100 to 170 mg/dl with worse validity. Most of the values were 130 and 140 mg/dl. The cutoff values of body weight index were constant in all clusters and showed greater validity than those for triglyceride. They were 115% or 120%. Their accuracy for the prediction of fatty liver was positively correlated with its prevalence. However, their accuracy was lower than 70% in non-diabetic females. We conclude that body weight index is a good parameter for prediction of fatty liver especially in the high risk groups and we recommend that health-determining cutoff values of serum triglyceride and body weight index should be set at 130 mg/dl and 115%, respectively.

Adult↗

PubMed2005

[Relationship between the severity of liver damage and the serum leptin level for nonalcoholic fatty liver disease].

BACKGROUND/AIMS: Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of conditions that are mainly characterized histologically by macrovesicular hepatic steatosis. There are two histologic patterns of NAFLD: simple steatosis alone and steatohepatitis. The factors leading from simple steatosis to nonalcoholic steatohepatitis (NASH) are still obscure. The datas from several studies have suggested that leptin could be involved in the progression from hepatic steatosis to steatohepatitis including the fibrosis. We evaluated serum leptin levels in patients with NAFLD to determine whether any relationships existed between the leptin levels and the severity of hepatic inflammation or fibrosis. METHODS: We studied 62 patients with NAFLD who were diagnosed at the Hallym University Sacred Heart Hospital from July 2001 to May 2004. We measured the serum leptin level in all cases and liver biopsy samples were obtained from 31 cases. The liver biopsy specimens were graded according to methods described by Brunt. Spearman rank correlations were used to detect the associations between the serum leptin and the various anthropometric and biochemical variables. The relationship between the histologic severity and the serum leptin level was evaluated with logistic regression analysis. RESULTS: Serum leptin levels correlated with insulin, c-peptide, ALT and homeostasis model assessment insulin resistance, but not with BMI, age and gender. Serum leptin level also correlated with hepatic fibrosis, but not with hepatic steatosis or inflammation. However, the serum leptin level was not a significant independent predictor of the grade of hepatic steatosis, inflammation and fibrosis on the univariate analysis. CONCLUSIONS: The serum leptin level was not an independent predictor of the severity of liver damage in NAFLD.

Adolescent↗

PubMed1999

Association of nonalcoholic fatty liver disease with insulin resistance.

BACKGROUND AND PURPOSE: Nonalcoholic fatty liver disease is frequently associated with type 2 diabetes mellitus, obesity, and dyslipidemia, but some patients have normal glucose tolerance or normal weight. We tested the hypothesis that there is an association between nonalcoholic fatty liver disease and insulin resistance that is independent of diabetes and obesity. SUBJECTS AND METHODS: We measured anthropometric and metabolic variables in 46 patients with chronically elevated serum aminotransferase levels, "bright liver" on ultrasound scan, and normal glucose tolerance. Indexes of insulin resistance and secretion were determined using the homeostasis model assessment method. They were compared with 92 normal subjects who were matched for age and sex. RESULTS: Patients with nonalcoholic fatty liver disease were characterized by fasting and glucose-induced hyperinsulinemia, insulin resistance, postload hypoglycemia, and hypertriglyceridemia. Insulin resistance [odds ratio (OR) = 15 per percent increase, 95% confidence interval (CI): 3.0 to 70], fasting triglyceride level (OR = 3.1 per mmol/liter increase, 95% CI: 1.1 to 8.9), 180-minute blood glucose level (OR = 4.3 per mmol/ liter decrease, 95% CI: 1.6 to 12), and average insulin concentration in response to oral glucose (OR = 3.0 per 100 pmol/liter increase, 95% CI: 1.5 to 6.2) were independently associated with nonalcoholic fatty liver disease. The exclusion of overweight and obese subjects did not change the results. CONCLUSION: Nonalcoholic fatty liver disease is associated with insulin resistance and hyperinsulinemia even in lean subjects with normal glucose tolerance. Genetic factors that reduce insulin sensitivity and increase serum triglyceride levels may be responsible for its development.

Adolescent↗

PubMed2005

Pulmonary fat embolism induced by exposure to high ambient temperature in rats with a fatty liver.

The aim of this study was to investigate whether a fatty liver contributes to pulmonary embolism under a high ambient temperature. As an experimental model, we exposed fatty liver rats to a high temperature (45 degrees C) and then looked for fat emboli in the alveolar capillaries using the fat-staining method. Fat emboli were detected in the alveolar capillaries of the fatty liver rats, but not in those of the normal liver rats. Moreover, the degree of pulmonary fat embolism tended to become more severe in proportion to the severity of the fatty liver. In addition, fat emboli did not appear at a core body temperature of 40 degrees C, but were detected at a core body temperature of 44 degrees C. From these results, we conclude that a fatty liver may contribute to the formation of pulmonary fat embolism and that high temperatures act as a trigger for the onset of pulmonary embolism. Moreover, it is possible that fatty liver affects the development of heat stroke induced by exposure to a high ambient temperature and that pulmonary fat embolism is a significant finding which helps to enable a diagnosis of heat stroke in autopsy cases.

Animals↗

PubMed2005

Prevalence of and risk factors for nonalcoholic fatty liver disease: the Dionysos nutrition and liver study.

The prevalence of and the risk factors for fatty liver have not undergone a formal evaluation in a representative sample of the general population. We therefore performed a cross-sectional study in the town of Campogalliano (Modena, Italy), within the context of the Dionysos Project. Of 5,780 eligible persons aged 18 to 75 years, 3,345 (58%) agreed to participate in the study. Subjects with suspected liver disease (SLD), defined on the basis of elevated serum alanine aminotransferase (ALT) and gamma-glutamyl-transferase (GGT) activity, hepatitis B surface antigen (HBsAg), or hepatitis C virus (HCV)-RNA positivity, were matched with randomly selected subjects of the same age and sex without SLD. A total of 311 subjects with and 287 without SLD underwent a detailed clinical, laboratory, and anthropometrical evaluation. Fatty liver was diagnosed by ultrasonography, and alcohol intake was assessed by using a 7-day diary. Multinomial logistic regression was used to detect risk factors for normal liver versus nonalcoholic fatty liver disease (NAFLD) and for alcoholic fatty liver (AFLD) versus NAFLD. The prevalence of NAFLD was similar in subjects with and without SLD (25 vs. 20%, P = .203). At multivariable analysis, normal liver was more likely than NAFLD in older subjects and less likely in the presence of obesity, hyperglycemia, hyperinsulinemia, hypertriglyceridemia, and systolic hypertension; AFLD was more likely than NAFLD in older subjects, males, and in the presence of elevated GGT and hypertriglyceridemia, and less likely in the presence of obesity and hyperglycemia. In conclusion, NAFLD is highly prevalent in the general population, is not associated with SLD, but is associated with many features of the metabolic syndrome.

Adult↗

PubMed1994

Recombinant liver fatty acid binding protein interacts with fatty acyl-coenzyme A.

Rat liver fatty acid binding protein (L-FABP) and rat intestine fatty acid binding protein (I-FABP) are homologous proteins which are both found in intestinal epithelial cells. It was once well accepted that liver fatty acid binding protein bound fatty acyl-CoAs, but the recent finding of a novel acyl-CoA binding protein (ACBP) in preparations of L-FABP has challenged the role of FABPs in acyl-CoA metabolism. Prior to the discovery of ACBP, L-FABP preparations from liver were shown to modulate the rate of fatty acyl-CoA synthesis (Burrier et al., 1987) and their conversion to phospholipids (Bordewick et al., 1989). Studies using FABPs free of ACBP are needed to determine the role of I-FABP and L-FABP in fatty acyl-CoA metabolism. In this study, highly pure recombinant L-FABP and I-FABP were used first to establish binding to fatty acyl-CoAs and then to examine the effects of these FABPs on microsomal phosphatidic acid synthesis. The standard Lipidex-1000 binding assay using [14C]oleoyl-CoA and a new fluorescence binding assay using the fluorescent fatty acyl-CoA cis-parinaroyl-CoA were used to determine binding. The results of these assays indicate that L-FABP binds fatty acyl-CoAs at two sites with a high-affinity Kd = 3-14 microM. These binding assays showed that I-FABP has a much lower affinity for fatty acyl-CoAs than does L-FABP. Furthermore, in vitro only L-FABP significantly increases the rate of incorporation of oleoyl-CoA into lysophosphatidic acid and phosphatidic acid.

Acyl Coenzyme A↗

PubMed1996

[Quantitative evaluation of 99mTc-GSA for fatty liver and ischemia-reperfusion injury in rats].

99mTc-GSA (GSA) liver scintigraphy was performed in rats with fatty liver and ischemia-reperfusion injury to study the usefulness of GSA in evaluating these pathological processes. Fatty liver was produced by feeding rats a choline-deficient diet. The rats with fatty liver were divided into five groups according to the length of the diet (controls, two weeks, six weeks, 10 weeks, and 12 weeks). In the rats dieted for two weeks and six weeks, regional hepatic ischemia was also induced by clamping the left hepatic artery and the left portal vein for 10 minutes, then reperfusion was performed for 15 minutes. GSA was administered via the IVC.t90, or the time at which the liver time activity curve reached ninety percent of its peak value, was used as an index of GSA hepatic uptake, Ku and Kd, determined by two compartment analysis, were also used as indices. In rats of the fatty liver group, we confirmed microscopically that various degrees of fatty infiltration existed according to the diet period, and t90 became significantly longer according to the severity of fatty infiltration. Ku and Kd also decreased according to the severity of fatty infiltration. In the rats with fatty infiltration and ischemia-reperfusion injury, t90 also increased according to the severity of fatty infiltration, becoming longer than in the rats without ischemia-reperfusion injury. Quantitative analysis of GSA liver scintigraphy was useful for evaluating fatty liver and ischemia-reperfusion injury.

Animals↗

PubMed1995

[Uncomplicated second pregnancy following acute fatty liver of pregnancy].

Acute fatty liver is a rare but usually severe and frightening complication of the last trimester of pregnancy. Many patients therefore do not want or are warned against having another child. This report adds another case of successful consecutive pregnancy to the 28 documented cases in 24 patients. On the other hand, only 2 recurrences have been reported. Therefore, the wish for another pregnancy may be supported, provided the gravida is well informed and the necessary (bi)weekly clinical and laboratory checks are carried out in the last trimester (liver tests, uric acid, prothrombin time and, in case of doubt, further coagulation tests including antithrombin III).

Adult↗

PubMed1995

Role of Kupffer cells in failure of fatty livers following liver transplantation and alcoholic liver injury.

Kupffer cells have been implicated in mechanisms of pathophysiology following liver transplantation. Recently, postoperative injury in ethanol-induced fatty liver has been evaluated because fatty livers often fail following transplantation. The low-flow, reflow liver perfusion model was used to study the role of Kupffer cells (KC) in reperfusion injury to fatty livers from rats fed a diet containing ethanol for 4-5 weeks. Treatment with GdCl3, which selectively destroys KC, decreased cell death significantly. Thus, destruction of KC minimized hepatic reperfusion injury, most likely by inhibiting free radical formation and improving microcirculation. Since it was demonstrated recently that destruction of KC prevented the hypermetabolic state observed with acute alcohol exposure, their involvement in events leading to alcohol-induced liver disease was investigated. In rats exposed to ethanol continuously via intragastric feeding for up to 4 weeks, GdCl3 treatment prevented elevation of aspartate aminotransferase (AST) and dramatically reduced the average hepatic pathological score. These results indicate that KC participate in the early phases of alcohol-induced liver injury. Endotoxaemia occurs in alcoholics and activates KC; therefore, we evaluated the effect of minimizing bacterial endotoxin by intestinal sterilization with the antibiotics polymyxin B and neomycin. Antibiotics diminished plasma endotoxin levels significantly and prevented ethanol-induced increases in AST values. These results indicate that endotoxin is involved in the mechanism of ethanol-induced liver injury. A six-line radical spectrum was detected with electron paramagnetic resonance spectroscopy in bile from alcohol-treated rats which was blocked by GdCl3. The free radical adducts had hyperfine coupling constants characteristic of lipid-derived free radical products. In conclusion, these studies demonstrate that KC are involved in reperfusion injury to ethanol-induced fatty livers and hepatic injury due to long-term treatment with ethanol.

Animals↗

PubMed2002

Absence of the G1528C (E474Q) mutation in the alpha-subunit of the mitochondrial trifunctional protein in women with acute fatty liver of pregnancy.

Acute fatty liver of pregnancy (AFLP) is a rare and dreaded complication of pregnancy, almost exclusively seen in the third trimester. The histopathologic features of AFLP closely resemble those seen in metabolic disorders characterized by deficiency of fatty acid oxidative enzymes. Several reports have established a strong association between AFLP in the mother and fetal deficiency of the enzyme long-chain L-3-hydroxyacyl-CoA dehydrogenase (LCHAD). However, these studies have an inevitable selection bias resulting from ascertainment through an affected infant, rather than an unselected population of patients with AFLP. We retrospectively examined a series of 10 women with pregnancies complicated by AFLP to determine the prevalence of the common LCHAD mutation (G1528C) in this population. The existing LCHAD primers, which produce a 640-bp amplicon (IJlst L, Ruiter JP, Hoovers JM, Jakobs ME, Wanders RJ: J Clin Invest 98:1028-1033, 1996), were modified to make them amenable to analysis of fragmented DNA obtained from microdissected formalin-fixed material. None of the patients were found to harbor the common G1528C mutation. It is likely that AFLP arising in the context of fetal LCHAD deficiency represents only one of the possible etiologies for this uncommon disorder, and the metabolic basis of AFLP is more heterogeneous than previously believed.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed2000

Do NSAIDs contribute to acute fatty liver of pregnancy?

Acute fatty liver of pregnancy (AFLP) and the childhood encephalopathy known as Reye's syndrome are both characterised by microvesicular steatosis. Mothers with AFLP are frequently heterozygous for a mutation which reduces the activity of the trifunctional protein (TP) of fatty-acid oxidation. Several lines of evidence suggest that blockade of fatty-acid oxidation may also be the underlying cause of Reye's syndrome, and epidemiological studies have identified aspirin taken during a viral illness as a contributing factor to the development of the disease. The hypotheses are presented:* that children with Reye's syndrome may also be heterozygous for TP mutation, and* that inhibition of the residual long-chain fatty-acid oxidation by NSAIDs including aspirin precipitates the similar symptoms observed in patients with Reye's syndrome and AFLP. Identification of NSAIDs as candidates for the unidentified factor which precipitates AFLP suggests that avoidance of NSAIDs during pregnancy may lead to a reduction in the incidence of this life-threatening disease.

Anti-Inflammatory Agents, Non-Steroidal↗