Apolipoprotein E Gene Polymorphism in Nonalcoholic Fatty Liver Disease

The aim of this study was to evaluate the relationship between apolipoprotein E gene polymorphism and nonalcoholic fatty liver disease. The study group consisted of 237 nonalcoholic fatty liver disease patients who were detected by ultrasonography and 201 controls with ultrasonographically normal livers. DNA amplifications were performed by polymerase chain reaction technique and apolipoprotein E genotypes were evaluated after digestion with CfoI restriction enzyme. Serum levels of glucose, lipids, lipoproteins, and apolipoproteins were measured in all subjects. Additionally, viral hepatitis markers, liver enzymes, and body mass index were assessed. Patients were found to have significantly higher triglyceride, glucose, aspartate aminotrasferase, alanine aminotransferase, and γ-glutamyltransferase levels and lower high-density lipoprotein cholesterol and apolipoprotein (a) levels than controls (P<0.05). There were no statistically significant differences in genotypes and allele frequencies between all patients and controls. Comparing nonobese patients with controls, the frequencies of allele ε2 and genotype ε2ε3 were statistically significantly different in the controls (P = 0.04 and P = 0.01, respectively). In conclusion, occurrence of the ε2 allele and ε2ε3 genotype may be protective against development of nonalcoholic fatty liver disease.     

A Decreased Response to Resistin in Mononuclear Leukocytes Contributes to Oxidative Stress in Nonalcoholic Fatty Liver Disease

Digestive Diseases and Sciences - Deregulation of immune response and oxidative stress contribute to nonalcoholic fatty liver disease (NAFLD) pathogenesis. Resistin is a physiological modulator of...     

Nonalcoholic Fatty Liver Disease after Liver Transplant

Nonalcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease in the world. The rising prevalence of nonalcoholic steatohepatitis (NASH) has led to a 170% increase in NASH cirrhosis as the listing indication for liver transplantation from 2004 to 2013. As of 2018, NASH has overtaken hepatitis C as an indication for liver transplantation in the USA. After liver transplantation, the allograft often develops recurrent NAFLD among patients with known NASH cirrhosis. In addition to recurrent disease, de novo NAFLD has been reported in patients with other indications for liver transplantation. In this review, we will discuss the risk factors associated with recurrent and de novo NAFLD, natural course of the disease, and management strategies after liver transplantation.     

人体脂肪／非脂成分比值与非酒精性脂肪肝关系的横断面研究

我国脂肪肝发病率呈逐年增长趋势且主要与肥胖症而非酒精滥用有关．寻找测量简便的非酒精性脂肪性肝病（NAFLD）预测指标具有重要意义。目的：探讨反映人体脂肪蓄积程度的脂肪／非脂成分比值（FFR）与非酒精性脂肪肝的关系。方法：以1025例上海市公务员为研究对象行横断面研究,调查和检测内容包括人口统计学资料、体质指数（BMI）、腰围（WC）、有无脂肪肝、人体成分分析、空腹血糖（FPG）、三酰甘油（TG）、高密度脂蛋白胆固醇（HDL-C）等,以单因素和多因素非条件logistic回归分析FFR与非酒精性脂肪肝的关系。结果：脂肪肝组与非脂肪肝组FFR的中位数和四分位数间距分别为0．39（0．33,0．45）和0．34（0．28,0．40）,组间差异有统计学意义（P〈0．001）。根据FFR的四分位数将研究对象按FFR由低至高分为四组,以FFR最低组为参照,调整性别、年龄、BMI、WC、FPG、TG、HDL-C因素后,各组发生脂肪肝的0R（95％CI）分别为1．37（0．82,2．28）、1．80（1．06,3．07）、2．59（1．44．4．67）．脂肪肝发生风险随FFR的增高呈上升趋势（trendP〈O．001）。结论：FFR增高与非酒精性脂肪肝相关．两者间存在剂量．反应关系．     

Therapeutic Options in Nonalcoholic Fatty Liver Disease

Opinion statement Nonalcoholic fatty liver disease, an entity that includes nonalcoholic steatohepatitis, is typically a benign, indolent condition. However, in a subset of patients, the clinical course may progress to advanced cirrhosis, end-stage liver disease, or hepatocellular carcinoma. Unfortunately, the pathogenesis, natural history, and potential therapies for these disorders remain poorly understood. Identifying patients who should be targeted for potential treatment remains difficult. Liver biopsy should be considered to assess the degree of hepatic inflammation and fibrosis, because physical examination findings, biochemical parameters, and the results of radiographic studies have been shown to correlate poorly with the severity of steatohepatitis and fibrosis. Although there is some evidence suggesting that obesity, diabetes mellitus, older age, and perhaps an aspartate transaminase:alanine aminotransaminase ratio higher than 1 may be predictors of more advanced fibrosis, histology remains the gold standard. Most patients with simple hepatic steatosis appear to follow a benign course and probably do not require aggressive therapy. Conversely, patients with steatohepatitis with extensive inflammation and fibrosis are the patients who are most likely to benefit from effective therapies. The most commonly recommended treatment is weight loss. Existing data suggest that rapid weight loss may promote hepatic inflammation and fibrosis; therefore, gradual weight loss should be recommended. Large, randomized, controlled trials evaluating the long-term histologic impact and clinical outcomes of weight loss strategies are lacking. Potentially promising pharmacologic therapies include insulin-sensitizing oral hypoglycemic agents such as metformin and the thiazolidenediols, antihyperlipidemic agents such as gemfibrozil or 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, vitamin E and other antioxidants, ursodeoxycholic acid, and betaine. As with weight loss, data regarding the efficacy of these pharmacologic options are limited. In addition, there are no widely accepted guidelines to help direct the clinician in the optimal use of these agents in patients with nonalcoholic fatty liver diseases.     

Iron Metabolism in Nonalcoholic Fatty Liver Disease

Non-Alcoholic Fatty Liver Disease (NAFLD) is a common worldwide clinical and major public health problem affecting both adults and children in developed nations. Increased hepatic iron stores are observed in about one-third of adult NAFLD patients. Iron deposition may occur in parenchymal and/or non-parenchymal cells of the reticuloendothelial system (RES). Similar patterns of iron deposition have been associated with increased severity of other chronic liver diseases including HCV infection and dysmetabolic iron overload, suggesting there may be a common mechanism for hepatic iron deposition in these diseases. In NAFLD, iron may potentiate the onset and progression of disease by increasing oxidative stress and altering insulin signaling and lipid metabolism. The impact of iron in these processes may depend upon the sub-cellular location of iron deposition in hepatocytes or RES cells. Iron depletion therapy has shown efficacy at reducing serum aminotransferase levels and improving insulin sensitivity in subjects with NAFLD.     

Computed Tomography in Nonalcoholic Fatty Liver Disease

The value and/or limitations of computed tomography (CT) in assessment of hepatosteatosis are not well studied in nonalcoholic fatty liver disease (NAFLD). We prospectively evaluated the accuracy of CT in assessing the amount of hepatosteatosis in NAFLD patients and the impact of demographic and histopathologic variables on CT images. Forty patients with biopsy-proven NAFLD were eligible. Of these, 10 exhibited hepatic iron overload. Liver and spleen attenuation measurements were obtained and spleen-minus-liver attenuation difference (ΔS–LA) was calculated. A good correlation between ΔS–LA and pathological hepatosteatosis was observed (r = 0.837, P < 0.0001). Liver iron overload did not affect this correlation, although the mean ΔS–LA was significantly lower in patients with iron overload. No correlation was detected between ΔS–LA and hepatic inflammation, fibrosis, or body mass index. We conclude that ΔS–LA derived from CT may be a useful tool for predicting the amount of hepatosteatosis in NAFLD patients as it is not affected by various individual factors.