非酒精性脂肪性肝病的研究进展

非酒精性脂肪性肝病经历由非酒精性单纯性脂肪肝发展至非酒精性脂肪性肝炎和肝硬化或原发性肝癌的缓慢过程,并与心血管病的发生关系密切.本文针对非酒精性脂肪性肝病的流行病学、发病机制、诊断和治疗等的研究进展进行综述.     

线粒体功能不全与非酒精性脂肪性肝病

非酒精性脂肪性肝病（NAFLD）是遗传、环境、代谢、应激相关因素所致的一种慢性肝脏疾病,包括单纯性脂肪肝、脂肪性肝炎和脂肪性肝硬化三种类型。NAFLD的发病机制复杂,     

解偶联蛋白2与非酒精性脂肪肝

非酒精性脂肪性肝病(NAFLD)包括单纯性脂肪肝及脂肪性肝炎，后者可以进展为肝纤维化和肝硬化，其发病机制尚不十分清楚。解偶联蛋白2(uncoupling protein-2，UCP2)由于其在NAFLD中的独特作用而日益受到学者的重视。现就UCP2在非酒精性脂肪性肝病中发生的可能作用作一综述。     

丹参冻干粉治疗糖尿病非酒精性脂肪肝的疗效观察

非酒精性脂肪肝（NAFL）包括单纯性脂肪肝、脂肪性肝炎、脂肪性肝硬化3种类型,糖尿病合并非酒精性脂肪性肝已成为我国常见的慢性肝病之一,近年来发病率呈上升趋势.本研究应用丹参冻干粉治疗糖尿病非酒精性脂肪肝,取得了比较满意的疗效,现报道如下.     

非酒精性脂肪性肝病与2型糖尿病：关系及研究进展

非酒精性脂肪性肝病（non-alcoholic fatty liverdisease．NAFLD）是一种除外过量饮酒和其他明确损肝因素所致的、以肝脏脂肪积聚为主要病理表现的慢性肝脏疾病．其疾病谱包括非酒精性单纯性脂肪肝、非酒精性脂肪性肝炎（non-alcoholic steatohepatitis．NASH）及其相关的肝硬化和肝细胞癌。非酒精性单纯性脂肪肝是一种良性病变     

非酒精性脂肪性肝病血清炎性反应因子含量变化及意义

非酒精性脂肪性肝病(NAFLD)包括单纯性脂肪肝、脂肪性肝炎、脂肪性肝纤维化等[1],其发病机制尚未完全阐明.外周血自然杀伤T(NKT)细胞比例变化与NAFLD有关[2].     

非酒精性脂肪性肝病与肝癌关系研究进展

随着生活水平提高,生活习惯与饮食结构的改变,非酒精性脂肪性肝病的发病率在不断增加。非酒精性脂肪性肝病包括一系列的疾病谱:单纯性脂肪肝、脂肪性肝炎、脂肪性肝纤维化及脂肪性肝硬化。肝细胞癌是脂肪性肝硬化的严重后果。因此,非酒精性脂肪性肝病与肝细胞癌之间存在着重要关系。本文就非酒精性脂肪性肝病与肝细胞癌关系的研究进展总结如下。     

非酒精性脂肪性肝病的无创诊断进展

现代社会由于肥胖的高度流行,与其相关的非酒精性脂肪性肝病（NAFLD）的患病率不断升高。从疾病的发展而言,非酒精性脂肪性肝病疾病谱包括单纯性肝脂肪变、非酒精性脂肪性肝炎（NASH）及脂肪性肝硬化。目前认为单纯性肝脂肪变为良性病变,而非酒精性脂肪性肝炎则易进展成为肝硬化及肝癌。     

脂肪性肝病研究新进展

<正>脂肪性肝病包括酒精性脂肪性肝病(ALD)和非酒精性脂肪性肝病(NAFLD)两大类。ALD包括单纯性脂肪肝、酒精性肝炎、酒精性肝纤维化及肝硬化;NAFLD包括单纯性脂肪肝(NAFL)、非酒精性脂肪肝性肝炎(NASH)、非酒精性脂肪性肝纤维化及肝硬化等。目前,全球脂肪性肝病的发病率逐年增多,尤其以发达国家和地区为甚。NAFLD还与2型糖尿病、心血管疾病、代谢综合征等疾病密切相     

非酒精性脂肪性肝病分子机制研究进展

非酒精性脂肪性肝病(NAFLD)是一种以肝细胞脂肪变性和脂质沉积为特征,但无过量饮酒史的临床综合征。NAFLD疾病谱包括非酒精性单纯性脂肪肝、非酒精性脂肪性肝炎(NASH)、NASH相关肝纤维化和肝硬化。NAFLD的发病机制较为复杂,至今尚未完全阐明。本文就近年NAFLD分子机制研究的新进展,包括胰岛素抵抗(IR)、肝脂肪变性、氧化应激等方面作一综述。     

Noninvasive diagnostic criteria for nonalcoholic steatohepatitis based on gene expression levels in peripheral blood mononuclear cells

Journal of Gastroenterology - Nonalcoholic fatty liver disease (NAFLD) consists of nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH); the latter progresses to liver cirrhosis...     

无创诊断和评估非酒精性脂肪性肝炎研究进展*

非酒精性脂肪性肝病（NAFLD）主要包括单纯性脂肪肝（NAFL)、非酒精性脂肪性肝炎（NASH）、相关肝硬化和肝细胞癌。相对于NAFL,NASH更易发展为肝硬化和肝癌,故早期诊断并对其干预尤为重要。近年来,多项无创诊断方法的出现致力于替代肝脏穿刺活检,主要包括血清学和影像学检查等,本文就无创性诊断和评估NASH作一综述。     

血管内皮生长因子与非酒精性脂肪性肝病

非酒精性脂肪性肝病（NAFLD）是影响公共健康的全球性疾病,其病理变化可向非酒精性单纯性脂肪肝（NAFL）、脂肪性肝炎（NASH）甚至脂肪性肝硬化（FLC）发展。虽然NAFLD的这些病理进展机制尚未明确,但仍有一些实验研究提示了可能的诱发机制。其中血管内皮生长因子（VEGF）在促进NAFLD肝脏炎症、肝纤维化中发挥着重要的作用。本文就VEGF与NAFLD关系的研究进展予以综述。     

Nonalcoholic fatty liver disease – current status and future directions

Nonalcoholic fatty liver disease (NAFLD) has emerged as the most common chronic liver disease worldwide with a reported prevalence ranging 6–33%, depending on the studied populations. It encompasses a spectrum of liver manifestations ranging from simple steatosis (also known as nonalcoholic fatty liver, NAFL) to nonalcoholic steatohepatitis (NASH), fibrosis and cirrhosis, which may ultimately progress to hepatocellular carcinoma. NAFLD is strongly associated with the components of metabolic syndrome, mainly obesity and type 2 diabetes mellitus. NAFLD patients are at increased risk of liver‐related as well as cardiovascular mortality. Current paradigm suggests a benign course for NAFL whereas NASH is considered to be the progressive phenotype. Although previously under‐recognized accumulating evidence suggests that NAFL may also progress, suggesting a higher number of patients at risk than previously appreciated. Liver biopsy remains the gold standard for definitive diagnosis, but the majority of patients can be diagnosed accurately by noninvasive methods. Approved therapies for NAFLD are still lacking and lifestyle modifications aiming at weight loss remain the mainstay of NAFLD treatment. Intensive research could identify insulin resistance, lipotoxicity and dysbiosis of the gut microbiota as major pathophysiological mechanisms, leading to the development of promising targeted therapies which are currently investigated in clinical trials. In this review we summarized the current knowledge of NAFLD epidemiology, natural history, diagnosis, pathogenesis and treatment and considered future directions.     

Klinische Bedeutung – Sinn und Unsinn – der Leberbiopsie bei NAFLD

Non-alcoholic fatty liver disease (NAFLD) comprises a spectrum ranging from bland non-alcoholic fatty liver (NAFL) to non-alcoholic steatohepatitis (NASH), liver cirrhosis, and hepatocellular cancer. Whereas “pure” NAFL rarely results in progressive liver disease, NASH can progress to liver cirrhosis in up to 25% of NASH patients. NAFL and NASH are both associated with an increased cardiovascular mortality, which represents the most important prognosis-limiting factor in both conditions. Diagnosis of NAFLD is based on clinical, biochemical, and sonographic findings. Liver biopsy is required for histologic distinction between NAFL and NASH. Because the therapeutic options for NASH are currently limited, liver biopsy has a rather limited value in the daily clinical management of NAFLD. Non-invasive laboratory and imaging methods (such as ultrasound elastography) may become increasingly important in the future.     

Serum Resistin as a Biomarker in Nonalcoholic Fatty Liver Disease: Is This a Road to be Taken?

Nonalcoholic fatty liver disease (NAFLD), which encompass-es a broad spectrum ranging from nonalcoholic fatty liver (NAFL) to nonalcoholic steatohepatitis (NASH...     

Symptoms of Obstructive Sleep Apnea in Patients with Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty liver disease (NAFLD) is a term often used to describe two related conditions: a relatively benign, nonalcoholic fatty liver (NAFL) and potentially aggressive, nonalcoholic steatohepatitis (NASH). Both conditions (NAFL and NASH) occur in the setting of peripheral insulin resistance. Recently, obstructive sleep apnea (OSA) has been proposed as an independent risk factor for insulin resistance. To date, few studies have documented the prevalence of OSA or symptoms of OSA (SOSA) in NAFLD patients. The objectives of this study were (1) to document the prevalence of SOSA in patients with NAFLD and (2) to determine whether prevalence rates for SOSA differ in NAFL versus NASH patients. One hundred ninety biochemically defined NAFLD patients (116 NAFL and 74 NASH), of whom 50 (18 NAFL and 32 NASH) had undergone liver biopsy, completed a Modified Berlin Sleep Apnea Questionnaire for SOSA. Risk factors for NAFLD were also documented in NAFL and NASH patients. Eighty-seven of the 190 (46%) NAFLD patients met questionnaire criteria for SOSA. The prevalence of SOSA was similar in both biochemically (45% versus 49%, respectively; P= 0.66) and histologically (39% versus 63%, respectively; P= 0.11) defined NAFL and NASH patients. Other risk factors for NAFLD such as body mass index, plasma cholesterol and triglyceride levels, and prevalence of diabetes were also similar in the two groups. Approximately one-half of NAFLD patients, whether NAFL or NASH, have SOSA. Further studies are required to determine whether a causal link exists between NAFLD and OSA.     

From the metabolic syndrome to NAFLD or vice versa?

The metabolic syndrome encompasses metabolic and cardiovascular risk factors which predict diabetes and cardiovascular disease (CVD) better than any of its individual components. Nonalcoholic fatty liver disease (NAFLD) comprises a disease spectrum which includes variable degrees of simple steatosis (nonalcoholic fatty liver, NAFL), nonalcoholic steatohepatitis (NASH) and cirrhosis. NAFLD is the hepatic manifestation of the metabolic syndrome, with insulin resistance as the main pathogenetic mechanism. Recent data indicate that hyperinsulinemia is probably the consequence rather than cause of NAFLD and NAFLD can be considered an independent predictor of cardiovascular disease. Serum free fatty acids derived from lipolysis of visceral adipose tissue are the main source of hepatic triglycerides in NAFLD, although hepatic de novo lipogenesis and dietary fat supply contribute to the pathogenesis of NAFLD. Approximately 10–25% NAFLD patients develop NASH, the evolutive form of hepatic steatosis. Presumably in a genetically predisposed environment, this increased lipid overload overwhelms the oxidative capacity and reactive oxygen species are generated, leading to lipid peroxidation, cytokine induction, chemoattraction of inflammatory cells, hepatic stellate cell activation and finally fibrogenesis with extracellular matrix deposition. No currently available therapies for NAFLD and NASH exist. Recently nuclear receptors have emerged as key regulators of lipid and carbohydrate metabolism for which specific pharmacological ligands are available, making them attractive therapeutic targets for NAFLD and NASH.     

Pathological Findings of NASH and NAFLD

Nonalcoholic fatty liver disease (NAFLD) is an increasingly common chronic liver disease worldwide. NAFLD comprises a variety of clinical and histopathological changes that can be broadly divided into nonalcoholic fatty liver (NAFL, simple steatosis) and nonalcoholic steatohepatitis (NASH). The differential diagnosis between NAFL and NASH is important because NASH is a more advanced form. This diagnosis therefore determines the prognosis and therapeutic management. At present the interpretation of NASH is made based on the histopathological features of steatohepatitis, i.e. ‘steatosis’, ‘lobular inflammation’, hepatocyte ‘ballooning, ‘Mallory‐Denk bodies’ and ‘fibrosis’. Here, we summarize the pathological findings guidelines for NASH as it was already published in 2015 in Japanese in the clinical guidebook organized by the Japan Society of Hepatology.     

A lipidomic analysis of nonalcoholic fatty liver disease

The spectrum of nonalcoholic fatty liver disease (NAFLD) includes a nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH). The specific types and amounts of lipids that accumulate in NAFLD are not fully defined. The free fatty acid (FFA), diacylglycerol (DAG), triacylglycerol (TAG), free cholesterol (FC), cholesterol ester, and phospholipid contents in normal livers were quantified and compared to those of NAFL and NASH, and the distribution of fatty acids within these classes was compared across these groups. Hepatic lipids were quantified by capillary gas chromatography. The mean (nmol/g of tissue) DAG (normal/NAFL/NASH: 1922 versus 4947 versus 3304) and TAG (13,609 versus 128,585 versus 104,036) increased significantly in NAFLD, but FFA remained unaltered (5533 versus 5929 versus 6115). There was a stepwise increase in the mean TAG/DAG ratio from normal livers to NAFL to NASH (7 versus 26 versus 31, P < 0.001). There was also a similar stepwise increment in hepatic FC (7539 versus 10,383 versus 12,863, P < 0.05 for NASH). The total phosphatidylcholine (PC) decreased in both NAFL and NASH. The FC/PC ratio increased progressively (0.34 versus 0.69 versus 0.71, P < 0.008 for both). Although the levels for linoleic acid (18:2n-6) and alpha-linolenic acid (18:3n-3) remained unaltered, there was a decrease in arachidonic acid (20:4n-6) in FFA, TAG, and PC (P < 0.05 for all) in NASH. Eicosapentanoic acid (20:5n-3) and docosahexanoic acid (22:6n-3) were decreased in TAG in NASH. The n-6:n-3 FFA ratio increased in NASH (P < 0.05). CONCLUSIONS: NAFLD is associated with numerous changes in the lipid composition of the liver. The potential implications are discussed.