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PubMedDate not supplied

The add-on effects of Gynostemma pentaphyllum on nonalcoholic fatty liver disease.

CONTEXT: Other than weight reduction by dieting or physical activity, there are no well-documented medical treatments for fatty liver disease. OBJECTIVE: To evaluate the efficacy of the add-on Gynostemma pentaphyllum (GP) in research subjects with nonalcoholic fatty liver disease. DESIGN: A randomized, single-blind, controlled clinical trial. SETTING: Hospital-based clinic. PATIENTS: Fifty-six research subjects who were diagnosed with nonalcoholic fatty liver by abdominal ultrasound scanning. INTERVENTIONS: The treatment group and the control group followed a controlled diet for 2 months. After 2 months, the treatment group continued to diet and received 80 mL GP extraction for 4 months; the control group continued to diet and received a placebo capsule for 4 months. MAIN OUTCOME MEASURES: Body mass index (BMI), biochemistry data, and fatty liver score were measured at baseline, at 2 months, and at 6 months. RESULTS: After 2 months of dieting, BMI and most biochemistry data decreased in both study groups. There were no significant differences in BMI or biochemistry data at month 2 between the 2 study groups. At month 6, BMI, triglyceride, aspartate aminotransferase (AST), alanine aminotransferase, alkaline phosphatase, insulin (ALP), insulin resistance index (HOMA-IR), and fatty liver score were reduced in both groups. The treatment group saw significant reductions in BMI, AST, ALP, insulin, and HOMA-IR, however. Changes in uric acid levels in the 2 groups from month 2 to month 6 were statistically significant (P = .028) CONCLUSION: GP is an effective adjunct treatment to diet therapy for patients with nonalcoholic fatty liver disease.

Adult↗
PubMed1996

Effect of taurine on the fatty liver of children with simple obesity.

This study elucidated the effect of taurine on fatty liver in simple obesity. Taurine was orally administered to 10 children with fatty liver. During taurine administration, the CT numbers of the liver, which were low in the beginning, increased. Serum ALT levels were improved, especially in those children whose weight was well controlled. Even in those who failed in weight control, serum ALT levels were slightly recovered. Ratios of glycine/taurine-conjugated bile acids were decreased. Thus, taurine was effective in treating fatty liver of children with simple obesity regardless of the success/failure of weight control. Taurine administration is considered to be helpful as an adjuvant therapy for fatty liver.

Adolescent↗
PubMed2003

Nonalcoholic fatty liver, steatohepatitis, and the metabolic syndrome.

Nonalcoholic fatty liver disease (NAFLD) has been associated with the insulin-resistance syndrome, at present defined as the metabolic syndrome, whose limits were recently set. We assessed the prevalence of the metabolic syndrome in 304 consecutive NAFLD patients without overt diabetes, on the basis of 3 or more criteria out of 5 defined by the U.S. National Institutes of Health (waist circumference, glucose, high-density lipoprotein [HDL]-cholesterol, triglycerides, and arterial pressure). The prevalence of the metabolic syndrome increased with increasing body mass index, from 18% in normal-weight subjects to 67% in obesity. Insulin resistance (Homeostasis Model Assessment method) was significantly associated with the metabolic syndrome (odds ratio [OR], 2.5; 95% CI, 1.5-4.2; P <.001). Liver biopsy was available in 163 cases (54%). A total of 120 patients (73.6%) were classified as having nonalcoholic steatohepatitis (NASH); 88% of them had a metabolic syndrome (vs. 53% of patients with pure fatty liver; P <.0001). Logistic regression analysis confirmed that the presence of metabolic syndrome carried a high risk of NASH among NAFLD subjects (OR, 3.2; 95% CI, 1.2-8.9; P =.026) after correction for sex, age, and body mass. In particular, the syndrome was associated with a high risk of severe fibrosis (OR, 3.5; 95% CI, 1.1-11.2; P =.032). In conclusion, the presence of multiple metabolic disorders is associated with a potentially progressive, severe liver disease. The increasing prevalence of obesity, coupled with diabetes, dyslipidemia, hypertension, and ultimately the metabolic syndrome puts a very large population at risk of forthcoming liver failure in the next decades.

Adult↗
PubMed2003

Increased susceptibility to nonalcoholic fatty liver disease in heterozygotes for the mutation responsible for hereditary hemochromatosis.

BACKGROUND: Insulin resistance is a key feature of nonalcoholic fatty liver disease. Patients with hereditary hemochromatosis, a disease characterized by progressive iron overload due, in most cases, to homozygosity for C282Y mutation in the HFE gene, have often decreased insulin sensitivity and release. AIMS: To determine whether increased iron parameters/heterozygosity for the mutations of the HFE gene confer susceptibility to nonalcoholic fatty liver disease. PATIENTS: One hundred and thirty-four consecutive Italian patients with clinical and ultrasonographic diagnosis of nonalcoholic fatty liver disease (82 with hyperferritinemia), half confirmed by liver biopsy. METHODS: Insulin was determined by radioimmunoassay. HFE gene mutations were determined by polymerase chain reaction and restriction fragment length polymorphism analysis. RESULTS: (1) Prevalence of C282Y HFE mutation was significantly higher in patients with nonalcoholic fatty liver disease compared to controls, the difference being more striking in patients with hyperferritinemia than in those without. (2) The presence of mild iron overload was associated with a lower insulin release. (3) Carriers of C282Y mutation developed nonalcoholic fatty liver disease despite lower body mass index and triglycerides. CONCLUSION: The mild iron overload associated with heterozygosity for C282Y HFE mutation confers susceptibility to nonalcoholic fatty liver disease, causing relative insulin deficiency.

Adult↗
PubMed2006

Transcriptional networks in a rat model for nonalcoholic fatty liver disease: a microarray analysis.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a common hepatic condition that may progress to end-stage liver disease. High-fat diets in animals reproduce many of the features found in nonalcoholic steatohepatitis. OBJECTIVE: To understand how various dietary or genetic factors influence the development of fatty liver and consequently NAFLD, we performed microarray-based expression profiling of genes, induced by fish oil and dextrose diet, a putative mediator of alcohol-like effects on the liver of the female rat. DESIGN: Male and age-matched female rats were fed fish oil and dextrose for 4 weeks. Hepatic RNA from each sample was extracted and used for microarray analysis. RESULTS: A large number of genes underwent significant changes in the female liver as compared to male controls. In the female rat liver, biological theme analysis demonstrated a shift in the transcriptional program which included upregulation of genes involved in lipid metabolism, chaperone activity, mitochondrial and oxidoreductase activity combined with downregulation of genes involved in nucleic acid metabolism. The differential expression of genes of interest identified by microarray technique was validated by real-time reverse transcription-polymerase chain reaction. Ingenuity computational pathway analysis tools were used to identify specific regulatory networks of genes operative in promoting liver injury. CONCLUSIONS: The use of networks stated above allowed us to identify genes involved in cell death, apoptosis, peroxisome proliferator-activated receptor alpha-regulated lipid metabolism and mitogen-activated protein kinase signaling pathways.

Animals↗
PubMed2005

Reduced intestinal fat absorptive capacity but enhanced susceptibility to diet-induced fatty liver in mice heterozygous for ApoB38.9 truncation.

Fatty liver is prevalent in apolipoprotein B (apoB)-defective familial hypobetalipoproteinemia (FHBL). Similar to humans, mouse models of FHBL produced by gene targeting (apob(+/38.9)) manifest low plasma cholesterol and increased hepatic triglycerides (TG) even on a chow diet due to impaired hepatic VLDL-TG secretive capacity. Because apoB truncations shorter than apoB48 are expressed in the intestine, we examined whether FHBL mice may have limited capacity for intestinal dietary TG absorption. In addition, we investigated whether FHBL mice are more susceptible to diet-induced hepatic TG accumulation. Fat absorption capacity was impaired in apoB38.9 mice in a gene dose-dependent manner. Relative fractional fat absorption coefficients for apob(+/+), apob(+/38.9), and apob(38.9/38.9) were 1.00, 0.96, and 0.71, respectively. To raise hepatic TG, we fed high-fat (HF) and low-fat (LF) pellets. Hepatic TG level was observed in rank order: HF > LF > chow. On both LF and HF, liver TG level was higher in the apob(+/38.9) than in apob(+/+). Hepatic TG secretion remained impaired in the apob(+/38.9) on the HF diet. Thus the FHBL mice are more susceptible to diet-induced fatty liver despite relatively reduced intestinal TG absorption capacity on a HF diet.

Animals↗
PubMed2004

Nonalcoholic fatty liver disease in the pediatric population.

Nonalcoholic fatty liver disease (NAFLD) covers the spectrum of features found in liver laden with macrovesicular fat and variable degrees of inflammation, cell injury, and fibrosis. By definition, NAFLD excludes those with significant ingestion of alcohol or alternative potential cause of steatohepatitis. NAFLD develops with rare exception in children who are obese. Given the rapid rise in prevalence of obesity in children globally, NAFLD is now recognized as the most common cause of liver disease in pediatrics. In obese individuals, Hispanic ethnicity and male gender appear to increase risk. Recent studies suggest that insulin resistance and oxidative stress are important in pathogenesis. Treatment trials are underway to determine if reduction of insulin resistance or oxidative stress will favorably affect outcome. This review summarizes what is known about pediatric nonalcoholic steatohepatitis in terms of prevalence, demographics, clinical presentation, histology,pathogenesis, and treatment. Important differences between pediatric and adult fatty liver disease are highlighted.

Adolescent↗
PubMed2003

Probiotics and antibodies to TNF inhibit inflammatory activity and improve nonalcoholic fatty liver disease.

Ob/ob mice, a model for nonalcoholic fatty liver disease (NAFLD), develop intestinal bacterial overgrowth and overexpress tumor necrosis factor alpha (TNF-alpha). In animal models for alcoholic fatty liver disease (AFLD), decontaminating the intestine or inhibiting TNF-alpha improves AFLD. Because AFLD and NAFLD may have a similar pathogenesis, treatment with a probiotic (to modify the intestinal flora) or anti-TNF antibodies (to inhibit TNF-alpha activity) may improve NAFLD in ob/ob mice. To evaluate this hypothesis, 48 ob/ob mice were given either a high-fat diet alone (ob/ob controls) or the same diet + VSL#3 probiotic or anti-TNF antibodies for 4 weeks. Twelve lean littermates fed a high-fat diet served as controls. Treatment with VSL#3 or anti-TNF antibodies improved liver histology, reduced hepatic total fatty acid content, and decreased serum alanine aminotransferase (ALT) levels. These benefits were associated with decreased hepatic expression of TNF-alpha messenger RNA (mRNA) in mice treated with anti-TNF antibodies but not in mice treated with VSL#3. Nevertheless, both treatments reduced activity of Jun N-terminal kinase (JNK), a TNF-regulated kinase that promotes insulin resistance, and decreased the DNA binding activity of nuclear factor kappaB (NF-kappaB), the target of IKKbeta, another TNF-regulated enzyme that causes insulin resistance. Consistent with treatment-related improvements in hepatic insulin resistance, fatty acid beta-oxidation and uncoupling protein (UCP)-2 expression decreased after treatment with VSL#3 or anti-TNF antibodies. In conclusion, these results support the concept that intestinal bacteria induce endogenous signals that play a pathogenic role in hepatic insulin resistance and NAFLD and suggest novel therapies for these common conditions.

Alanine Transaminase↗
PubMed1996

Effects of refeeding diets on emeriamine-induced fatty liver in fasting rats.

We recently reported that fatty liver and hypertriglyceridemia are easily induced by the administration of an inhibitor of fatty acid oxidation (emeriamine; (R)-3-amino-4-trimethylaminobutyric acid) to fasting rats, and that these conditions are not accompanied by the increased de novo synthesis of fatty acid [J. Nutr. Sci. Vitaminol., 42, 111-120, (1996)]. To study whether emeriamine-induced fatty liver is affected by nutrients during recovery from fatty acid oxidation inhibition, we fed rats with either a high-carbohydrate (HCHO) diet or a high-fat (HFAT) diet. Rats fed an HCHO diet following the administration of emeriamine showed a marked decrease in serum and hepatic triglycerides, and a marked increase in hepatic glycogen. The lower levels of serum and hepatic triglycerides were accompanied by decreased activities of the NADPH-generating enzymes such as malic enzyme and glucose-6-phosphate dehydrogenase. By contrast, rats fed an HFAT diet showed less significant changes in hepatic triglyceride and glycogen levels. These results suggest a reciprocal relationship between the triglyceride level and glycogen accumulation caused by HCHO diet during recovery from emeriamine.

Animals↗
PubMed1996

Study of the liver changes occurring in preeclampsia and their possible pathogenetic connection with acute fatty liver of pregnancy.

OBJECTIVE: The objective of the present study was to investigate liver involvement in preeclampsia on the basis of clinical, laboratory, and histological data and to detect a possible connection with fatty liver of pregnancy by the determination of microvesicular fatty infiltration of the liver. METHODS: The authors studied the liver changes in 10 patients with preeclampsia, observing the clinical and laboratory alterations, the macroscopic liver surface features by laparoscopy, and the presence of microvesicular fatty infiltration by specific lipid staining of hepatic tissue collected by needle biopsy. RESULTS: Macroscopy of the liver surface disclosed some degree of subcapsular liver hemorrhage in all cases; however, the hemorrhage was not related to the clinical and histological severity of the disease. Microvesicular fat droplets were observed in all patients, and the intensity of the fat deposition was not related to pressor levels, laboratory alterations, or the evolution of preeclampsia. CONCLUSIONS: The presence of fatty liver infiltration in all patients studied supports the idea that preeclampsia and acute fatty liver of pregnancy could be components of the same pathologic spectrum, with a probable, but still unproved, pathogenetic connection. The deficiency of the long chain 3-hydroxyacyl-coenzyme A dehydrogenase activity may be the determining factor in the evolution of the disease.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed2004

Insulin resistance and ferritin as major determinants of nonalcoholic fatty liver disease in apparently healthy obese patients.

OBJECTIVES: The aims of this study were to test the possible association between nonalcoholic fatty liver disease (NAFLD) and iron and insulin resistance, and to determine the prevalence of NAFLD in apparently healthy obese subjects. DESIGN: Cross-sectional, clinical epidemiologic study. SUBJECTS: A total of 210 apparently healthy obese patients, aged from 18 to 65 y, with a body mass index (BMI) of 28 kg/m2 or more, were enrolled in a body weight reduction program in our hospital. MEASUREMENTS: All the subjects underwent screening and preprogram examinations, including anthropometric data measurements, biochemistry testing, and ultrasonography of the liver. NAFLD was defined as fatty liver diagnosed by ultrasonography plus persistent elevation of alanine aminotransferase (ALT) levels. RESULTS: Of the 210 patients, 80% (168/210) had fatty liver. Persistent ALT elevation in two separate tests was further detected in 25.6% (43/168) of patients. Multiple logistic regression analysis showed waist circumference and insulin resistance to be independently associated with fatty liver. Serum ferritin level and insulin resistance were two major risk factors predicting NAFLD. CONCLUSION: The prevalence of NAFLD was 20.5% (43/210) in obese patients. As both hyperinsulinemia induced by insulin resistance and iron overload represented by ferritin elevation might damage hepatocytes, we concluded that these two factors were significantly associated with NAFLD in obese patients.\

Adolescent↗
PubMed2006

Nonalcoholic Fatty Liver Disease (NAFLD): Approach in the Adolescent Patient.

Nonalcoholic fatty liver disease (NAFLD) is a spectrum of liver disease whose hallmark is the accumulation of large-droplet fat in hepatocytes. This metabolic disorder occurs mainly in overweight or obese individuals. The disease mechanism involves hyperinsulinemia and hepatic insulin resistance, not ethanol abuse. NAFLD may be the hepatic manifestation of the "metabolic syndrome" classically associated with type 2 diabetes mellitus and cardiovascular disease. NAFLD ranges from simple steatosis, which is the least rapidly progressing disorder, to nonalcoholic steatohepatitis to cirrhosis, which can evolve to chronic liver failure. The high prevalence of NAFLD in children has been recognized only in the past 5 to 10 years, as rates of childhood obesity have soared. Accordingly, the best strategies for diagnosis and treatment of childhood NAFLD are a work in progress and remain controversial. Weight reduction through a healthy diet and regular medium-intensity exercise is the mainstay of current treatment. Few research data are available to guide pharmacologic therapy. Certain points regarding management of childhood NAFLD require emphasis: It is a serious liver disease that requires detailed clinical investigation. Other liver diseases causing fatty liver and/or abnormal liver tests, notably Wilson disease and chronic viral hepatitis, need to be excluded. Liver biopsy can provide critical diagnostic and staging information. Associated genetic or endocrine disorders need to be identified. Treatment should begin with a low-glycemic index diet that provides adequate nutrients but is low in harmful fats and eliminates foods causing postprandial hyperglycemia. Initially, this can target two to three problem foods so that it is easy for the adolescent to follow. Regular exercise suited to the capabilities and interests of the teenager should be added to the daily routine. Where possible, a team approach, including a dietician and psychologist, should be utilized, as adolescents do better in a supportive atmosphere. Optimal drug treatment requires further research: current front-runners are vitamin E and metformin. The roles of drugs that alter appetite and bariatric surgery for adolescents with NAFLD have not been determined.

Journal Article↗
PubMed1975

Effects of nutritional factors on the development of ethanol-induced fatty liver in KK and KK-Ay mice.

KK and KK-Ay mice developed a steady and reproducible fatty liver when they were given free access to an ethanol solution as a drinking fluid for 10 to 20 days. The present studies were undertaken to elucidate effects of nutritional factors on liver fat contents of the mice given water or ethanol solution. In contrast to cornstarch, sucrose tended to increase the liver fat of control mice. A higher concentration of dietary casein lowered the liver fat of control mice, whereas the dietary concentration of cottonseed oil did not significantly affect the liver rat levels either in control or ethanol groups. Thus the standard basal diets favorable for the development of the alcoholic fatty liver have been established, for example, 10% cottonseed oil, 25 and 30% casein, 58.4 and 53.4% cornstarch for KK (12-15 weeds old) and KK-Ay (5-10 weeks old), respectively. Neither choline, myoinositol, nor any lipotropic agent tested prevented the development of the alcoholic fatty liver. Unlike in rats, orotic acid did not induce a fatty liver but rather alleviated the ethanol-induced fatty liver in these mice.

Age Factors↗
PubMed2000

A study of fatty liver disease and plasma lipoproteins in a kindred with familial hypobetalipoproteinemia due to a novel truncated form of apolipoprotein B (APO B-54.5).

BACKGROUND/AIMS: Familial hypobetalipoproteinemia (FHBL) is a co-dominant disorder characterized by reduced plasma levels of low-density lipoproteins. It can be caused by mutations in the gene encoding apolipoprotein B-100 (apo B), leading to the formation of truncated apo Bs which have a reduced capacity to export lipids from the hepatocytes as lipoprotein constituents. Case reports suggest the occurrence of liver disease in FHBL, but there are no studies of liver involvement in FHBL with defined apo B gene mutations. The presence of fatty liver disease was investigated in a large FHBL kindred. METHODS: Plasma lipoprotein and apolipoprotein analysis, liver function tests, and apo B gene sequence were performed in 16 members of a FHBL kindred. The presence of fatty liver was assessed by ultrasound and computed tomography scanning. RESULTS: The proband, a non-obese heavy drinker male with hypobetalipoproteinemia, had steatohepatitis with fibrosis. He was heterozygous for a novel non-sense mutation of apo B gene producing a truncated apo B of 2745 amino acids (designated apo B-54.5, having half the size of normal apo B-100). Seven other members of his kindred carried apo B-54.5. Although all of them were hypolipidemic, their lipid levels showed a large inter-individual variability not accounted for by polymorphisms of genes involved in apo B metabolism. Four carriers (two heavy drinkers and two teetotallers), irrespective of their plasma lipid levels, had ultrasonographic evidence of fatty liver. In the other four carriers no evidence of fatty liver was found. CONCLUSIONS: In this kindred apo B-54.5 predisposes to fatty liver, which however may require some additional factors to become clinically relevant.

Apolipoproteins↗
PubMed2004

Oxidative stress in nonalcoholic fatty liver disease: pathogenesis and antioxidant therapies.

Nonalcoholic fatty liver disease is a common cause of chronic liver disease, a common finding on liver biopsy in those patients with abnormal blood transaminase levels, and a common cause of cryptogenic cirrhosis in the United States. The prevalence of this disorder is expected to rise with the increase in obesity, and the clinical spectrum can range from simple steatosis (fatty liver) to cirrhosis of the liver. Insulin resistance is thought to be pivotal for the development of steatosis, and oxidative stress may be a potential factor that can promote hepatic necroinflammation and fibrosis. Preliminary studies have examined the role of oxidative stress and antioxidants in animal and human studies of this disorder. Efforts to improve the hepatic antioxidant system could be achieved by optimizing the patient's diet, by supplementation with precursors for antioxidants, or by supplementation with essential metals and/or antioxidants. Randomized, controlled trials are required to examine these potential approaches using patients with this disorder.

Animals↗
PubMed1997

Glucose and insulin responses to glucagon injection in dairy cows with ketosis and fatty liver.

The purpose of this investigation was to study the metabolic situation in clinical cases of bovine ketosis and to diagnose additional diseases. Extensive clinical examination, clinical biochemistry, haematology and fine-needle aspiration biopsy of liver was performed on 17 ketotic and eight control dairy cows in the field, and on seven hospitalized hyperketonaemic fatty liver patients. Additional findings in the ketotic group were heat (n = 7), indigestion (n = 5), endometritis (n = 2), cystic ovaries (n = 1), and mastitis (n = 1), and in the fatty liver group displaced abomasum (n = 4), abomasal ulcers (n = 3), mastitis (n = 2), laminitis (n = 1), bronchopneumonia (n = 1), and hypomagnesaemia (n = 2). There were no additional findings in the control group. Aspartate aminotransferase (AST) and creatine kinase (CK) were elevated in the ketosis and fatty liver groups. Total bilirubin, gamma-glutamyl transferase (GGT) and glutamate dehydrogenase (GD) were elevated in the fatty liver group and in some animals in the ketosis group. Total bile acid was not different between the groups. The free fatty acid/cholesterol ratio was higher in the fatty liver group compared with the control and ketosis groups. There was no or only slight fatty degeneration of the liver cells in the control and ketosis groups. Glucose and insulin preinjection concentrations and changes from basal values after glucagon injection were significantly lower in the ketosis group if compared with the control group. The responses in the fatty liver animals after glucagon injection were more heterogeneous than in the control and ketosis animals, a sign of disturbance in the metabolic adaptation, which together with high free fatty acid (FFA) levels can lead to fatty liver in cows with concurrent diseases.

Animals↗
PubMed2005

Dietary factors alter hepatic innate immune system in mice with nonalcoholic fatty liver disease.

Dietary factors promote obesity and obesity-related disorders, such as fatty liver disease. Natural killer T (NKT) cells are components of the innate immune system that regulate proinflammatory (Th-1) and anti-inflammatory (Th-2) immune responses. Previously, we noted that NKT cells are selectively reduced in the fatty livers of obese, leptin-deficient ob/ob mice and demonstrated that this promotes proinflammatory polarization of hepatic cytokine production, exacerbating lipopolysaccharide (LPS) liver injury in these animals. In the current study, we show that hepatic NKT cells are also depleted by diets that induce obesity and fatty livers in wild-type mice, promoting Th-1 polarization of hepatic cytokine production and sensitization to LPS liver injury despite persistent leptin. Adult male C57BL6 mice fed diets containing high amounts of either fat or sucrose, or combined high-fat, high-sucrose, develop increased hepatic NKT cell apoptosis and reduced liver NKT cells. The hepatic lymphocytes are more Th-1 polarized with increased intracellular interferon gamma and tumor necrosis factor alpha. Mice fed high-fat diets also exhibit more liver injury, reflected by 2-fold greater serum alanine aminotransferase (ALT) than control animals after receiving LPS. In conclusion, when otherwise normal mice are fed with high-fat or sucrose diet, they become obese, develop fatty livers, and acquire hepatic innate immune system abnormalities, including increased NKT cell apoptosis. The latter reduces liver NKT cell populations and promotes excessive hepatic production of Th-1 cytokines that promote hepatic inflammation. These diet-induced alterations in the hepatic innate immune system may contribute to obesity-related liver disease.

Animals↗
PubMedDate not supplied

Serum vitamin-E levels and its relation to clinical features in nonalcoholic fatty liver disease with elevated ALT levels.

BACKGROUND: Oxidative stress and free oxygen radicals play an important role in the progression from simple fatty liver to steatohepatitis. Deficiency of antioxidants like vitamin-E has been reported to trigger this progression. The main aims of our study were to measure plasma vitamin-E levels in nonalcoholic fatty liver disease (NAFLD), to explain its relationship with biochemical parameters and to examine the possible therapeutic and prophylactic role of vitamin-E. METHODS: 52 patients with NAFLD and elevated liver function tests were enrolled. After 6 months of follow-up with a standard low-fat, low-calorie diet, changes in liver enzymes were evaluated. RESULTS: Deficiency of vitamin-E was detected in 16 patients with NAFLD. Homogenous echo pattern of the liver and attenuation was found to be significantly higher in the low vitamin-E group (p = 0.03). The low vitamin-E group had significantly higher levels of triglyceride (p = 0.02). After 6 months, patients in the low vitamin-E group did not respond to the diet and no decrease in ALT levels was detected (p = 0.04). CONCLUSION: This is the first study measuring the serum vitamin-E levels in nonalcoholic fatty liver disease. A correlation was found between low vitamin-E levels, high triglyceride levels, as well as sonographic findings, both of which are negative prognostic factors causing progression of fatty liver to steatohepatitis. Patients with low vitamin-E levels did not respond to a classical diet for fatty liver disease. Based on the data, we suggest that diet alone is not adequate for patients with fatty liver, and vitamin-E supplementation should be added.

Adult↗