Treatment of nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) is the most common cause for elevated liver enzymes in the developed nations. Beyond prevention programs which are of particular interest because of the increasing number of overweight children, treatment should be focussed on the most important risk factors, obesity and insulin resistance. As a consequence of elucidating the pathomechanisms of NAFLD, the number of potential therapeutic options increased. However, many studies investigating the therapeutic effect show shortcomings in at least one of the following points: lack of a serial liver biopsy, short term of treatment and limited number of included patients. The second generation insulin sensitizer piogiitazone and rosiglitazone show the most promising improvements in NAFLD, but weight gain and potential hepatotoxicity calls for attention. In conclusion, a general recommendation for the application of specific drugs cannot be given. Besides controlled clinical trials, weight reduction and physical activity to improve insulin sensitivity in obese patients should be the priority objective.     

Histopathology of nonalcoholic fatty liver disease

Histological analysis of liver biopsies remains a standard against which other methods of assessment for the presence and amount of hepatic injury due to nonalcoholic fatty liver disease(NAFLD) are measured.Histological evaluation remains the sole method of distinguishing steatosis from advanced forms of NAFLD,i.e.nonalcoholic steatohepatitis(NASH) and fibrosis.Included in the lesions of NAFLD are steatosis,lobular and portal inflammation,hepatocyte injury in the forms of ballooning and apoptosis,and fibros...     

Transition of an acronym from nonalcoholic fatty liver disease to metabolic dysfunction-associated fatty liver disease

Nonalcoholic fatty liver disease(NAFLD) is a global public health concern owing to its substantial contribution to chronic liver diseases. The disease is closely linked to metabolic syndrome(MS), suggesting a common biological pathway and shared disease mechanism for both ailments. Previous studies revealed a close relationship of NAFLD with the components of MS including abdominal obesity,dyslipidemia, hypertension, and hyperglycemia. Hence, a group of experts recently renamed NAFLD as metabolic dysfunction-associated fatty liver disease(MAFLD) in order to encompass a more appropriate pathogenesis of the disease.NAFLD was first named to describe a condition similar to alcoholic hepatitis in absence of significant alcohol consumption. However, knowledge pertaining to the etiopathogenesis of the disease has evolved over the past four decades. Recent evidence endorses NAFLD as a terminology of exclusion and suggests that it may often leads to misdiagnosis or inappropriate management of patients, particularly in clinical practice. On the other hand, the new definition is useful in addressing hepatic steatosis with metabolic dysfunction, which ultimately covers most of the patients with such illness. Therefore, it seems to be helpful in improving clinical diagnosis and managing high-risk patients with fatty liver disease. However, it is imperative to validate the new terminology at the population level to ensure a holistic approach to reduce the global burden of this heterogeneous disease condition.     

肠道益生菌对非酒精性脂肪肝的影响

目的探讨肠道菌群与非酒精性脂肪肝(NAFLD)的关系。方法对53例服用肠道益生菌的NAFLD患者和56例对照组患者进行服药前后肝脏的超声检查,抽血查血肌酐、尿素氮、总胆固醇、三酰甘油、空腹血糖,并同时对年龄和体质量指数(BMI)进行统计。结果服药前两组各项指标比较,差异无统计学意义(P0.05)。服药后肠道益生菌组和对照组比较,脂肪肝消退数明显增加,差异有统计学意义(P0.05)。服药前后两组比较,肠道益生菌组服药后较服药前脂肪肝消退数明显增加,差异有统计学意义(P0.01);而对照组各项指标比较,差异均无统计学意义(P0.05)。两组服药前后各种观察指标差值的比较,脂肪肝消退、中度脂肪肝减少数、总胆固醇、三酰甘油和尿素氮下降在肠道益生菌组差异有统计学意义(P0.05、P0.01)。结论口服益生菌可以降低NAFLD的发生,益生菌可能具有预防和治疗NAFLD的作用。     

Histopathology of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis

Nonalcoholic fatty liver disease (NAFLD), a hepatic manifestation of metabolic syndrome, is the most common chronic liver disease, and the prevalence is rapidly increasing worldwide. Nonalcoholic steatohepatitis (NASH), the severe form of NAFLD, can progress to liver cirrhosis and hepatocellular carcinoma (HCC). Although noninvasive clinical scores and image-based diagnosis for NAFLD have improved, histopathological evaluation of biopsy specimens remains the gold standard for diagnosing NAFLD/NASH. Steatosis, lobular inflammation, and hepatocellular ballooning are all necessary components for the diagnosis of NASH; fibrosis is also typically observed. Other histopathological abnormalities commonly observed in NASH include hepatocellular glycogenated nuclei, lipogranulomas, and acidophil bodies. The characteristics of pediatric NAFLD/NASH differ from adult NAFLD/NASH. Specifically, steatosis and portal inflammation are more severe in pediatric NAFLD, while intralobular inflammation and perisinusoidal fibrosis are milder. Although interobserver agreement for evaluating the extent of steatosis and fibrosis is high, agreement is low for intralobular and portal inflammation. A recently reported histological variant of HCC, steatohepatitic HCC (SH-HCC), shows features that resemble non-neoplastic steatohepatitis, and is thought to be strongly associated with underlying NASH. In this report, we review the histopathological features of NAFLD/NASH.     

Clinical differences between alcoholic liver disease and nonalcoholic fatty liver disease

Alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) are serious health problems worldwide. These two diseases have similar pathological spectra, ranging from simple hepatic steatosis to steatohepatitis, liver cirrhosis, and hepatocellular carcinoma. Although most subjects with excessive alcohol or food intake experience simple hepatic steatosis, a small percentage of individuals will develop progressive liver disease. Notably, both ALD and NAFLD are frequently accompanied by extrahepatic complications, including cardiovascular disease and malignancy. The survival of patients with ALD and NAFLD depends on various disease-associated conditions. This review delineates the clinical characteristics and outcomes of patients with ALD and NAFLD by comparing their epidemiology, the factors associated with disease susceptibility and progression, and the predictors and characteristics of outcomes. A comprehensive understanding of the characteristics and outcomes of ALD and NAFLD is imperative in the management of these chronic liver diseases.     

胰岛素抵抗与非酒精性脂肪性肝病

胰岛素抵抗(IR)在非酒精性脂肪性肝病(NAFLD)发病过程中起至关重要的作用.目前大量研究支持NAFLD“二次打击”学说,初次打击IR引起肝细胞单纯性脂肪变性,二次打击脂肪变的肝细胞发生成脂性转化,诱导炎性反应、氧化应激、内质网应激的发生,损伤肝细胞功能,加重IR,促进NAFLD发展.     

Mediterranean diet and nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease(NAFLD) is emerging as the most common chronic liver disease, and is characterized by a wide spectrum of fat-liver disorders that can result in severe liver disease and cirrhosis. Inflammation and oxidative stress are the major risk factors involved in the pathogenesis of NAFLD. Currently, there is no consensus concerning the pharmacological treatment of NAFLD. However, lifestyle interventions based on exercise and a balanced diet for quality and quantity, are considered the cornerstone of NAFLD management. Mediterranean diet(MD), rich in polyunsaturated fats, polyphenols, vitamins and carotenoids, with their anti-inflammatory and antioxidant effects, has been suggested to be effective in preventing cardiovascular risk factors. In adults, MD has also been demonstrated to be efficacious in reducing the risk of metabolic syndrome. However, few studies are available on the effects of the MD in both adult and pediatric subjects with NAFLD. Thus, the aims of the present narrative review are to analyze the current clinical evidence on the impact of MD in patients with NAFLD, and to summarize the main mechanisms of action of MD components on this condition.     

瘦素与非酒精性脂肪性肝病的关系

啮齿类动物胰岛分离的应用广泛 ,其方法也早已建立 ,但影响胰岛分离的因素较多 ,使获得足量、纯净、存活和功能良好的胰岛常较困难 ,且胰岛分离的稳定性和一致性亦难令人满意。因此 ,针对分离技术、纯化方法、分离剂、消化酶及消化条件等诸方面进行了广泛的改进 ,胰岛的收获量、纯度及活力等均有显著的提高。     

瘦素与非酒精性脂肪性肝病的关系

瘦素属于蛋白质激素.主要由白色脂肪组织分泌,由瘦素受体介导发挥生物学作用.最初发现其参与机体代谢调节,控制机体脂肪量.近年来发现其与非酒精性脂肪性肝病的关系密切,但研究结果并不一致.有学者研究发现非酒精性脂肪性肝病患者血清瘦素水平无明显提高,也有学者提出瘦素在非酒精性脂肪性肝病患者中显著提高,并在其发病中具有独立的重要作用,瘦素的抗脂毒性减弱及瘦素抵抗被认为是其中的重要环节.     

瘦素与非酒精性脂肪性肝病的关系

瘦素属于蛋白质激素.主要由白色脂肪组织分泌,由瘦素受体介导发挥生物学作用.最初发现其参与机体代谢调节,控制机体脂肪量.近年来发现其与非酒精性脂肪性肝病的关系密切,但研究结果并不一致.有学者研究发现非酒精性脂肪性肝病患者血清瘦素水平无明显提高,也有学者提出瘦素在非酒精性脂肪性肝病患者中显著提高,并在其发病中具有独立的重要作用,瘦素的抗脂毒性减弱及瘦素抵抗被认为是其中的重要环节.     

瘦素与非酒精性脂肪性肝病的关系

瘦素属于蛋白质激素.主要由白色脂肪组织分泌,由瘦素受体介导发挥生物学作用.最初发现其参与机体代谢调节,控制机体脂肪量.近年来发现其与非酒精性脂肪性肝病的关系密切,但研究结果并不一致.有学者研究发现非酒精性脂肪性肝病患者血清瘦素水平无明显提高,也有学者提出瘦素在非酒精性脂肪性肝病患者中显著提高,并在其发病中具有独立的重要作用,瘦素的抗脂毒性减弱及瘦素抵抗被认为是其中的重要环节.     

瘦素与非酒精性脂肪性肝病的关系

瘦素属于蛋白质激素.主要由白色脂肪组织分泌,由瘦素受体介导发挥生物学作用.最初发现其参与机体代谢调节,控制机体脂肪量.近年来发现其与非酒精性脂肪性肝病的关系密切,但研究结果并不一致.有学者研究发现非酒精性脂肪性肝病患者血清瘦素水平无明显提高,也有学者提出瘦素在非酒精性脂肪性肝病患者中显著提高,并在其发病中具有独立的重要作用,瘦素的抗脂毒性减弱及瘦素抵抗被认为是其中的重要环节.     

瘦素与非酒精性脂肪性肝病的关系

瘦素属于蛋白质激素.主要由白色脂肪组织分泌,由瘦素受体介导发挥生物学作用.最初发现其参与机体代谢调节,控制机体脂肪量.近年来发现其与非酒精性脂肪性肝病的关系密切,但研究结果并不一致.有学者研究发现非酒精性脂肪性肝病患者血清瘦素水平无明显提高,也有学者提出瘦素在非酒精性脂肪性肝病患者中显著提高,并在其发病中具有独立的重要作用,瘦素的抗脂毒性减弱及瘦素抵抗被认为是其中的重要环节.     

非酒精性脂肪性肝病与幽门螺杆菌感染的相关性

目的探讨非酒精性脂肪性肝病(NAFLD)与幽门螺杆菌(H.pylori)感染之间的关系。方法采用横断面研究方法,分析2011年于北京医院体检中心进行健康体检者中体检数据完整、进行13C-尿素呼气试验检测H.pylori及腹部超声检查的受试者14 373人(年龄≥18岁)的体检数据。应用非条件Logistic回归分析H.pylori感染状态与NAFLD的关系。结果 NAFLD及H.pylori感染检出率均在50~59岁年龄段最高,分别达46.27%和32.38%。NAFLD及H.pylori感染检出率随年龄变化趋势相同。NAFLD患者中H.pylori阳性者较H.pylori阴性者体质量指数(BMI)高、甘油三酯(TG)高,而高密度脂蛋白胆固醇(HDL-C)低(P0.05),肝功指标、血糖、尿酸无显著差异(P0.05)。H.pylori感染状态与NAFLD呈正相关(OR=1.265,95%CI:1.116~1.403)。结论H.pylori感染与NAFLD呈正相关,H.pylori感染可能是NAFLD发生的危险因素。     

Comparative redox status in alcoholic liver disease and nonalcoholic fatty liver disease

Purpose Altered redox status has been implicated in pathogenesis of alcoholic liver disease (ALD) as well as in nonalcoholic fatty liver disease (NAFLD). This study was planned to find the relative role of redox status in these two diseases. Methods A total of 44 patients with ALD and 32 patients with NAFLD and 25 apparently healthy controls were included in the study. Redox status was estimated by measuring oxidative stress (superoxide dismutase (SOD) and lipid peroxidation products as thiobarbituric acid reactive substances (TBARS)) and antioxidant status (ferric reducing ability of plasma (FRAP) and vitamin C). Results TBARS level was raised significantly in both ALD (3.5 (2.3–9.4) vs. 1.8 (0.5–4.1) nmol/ml; P = 0.0001) and NAFLD (5.1 (1–10.2) vs. 1.82 (0.51–4.1) nmol/ml; P = 0.0001) as compared with controls, but was not different between ALD and NAFLD. SOD was significantly higher in ALD as compared to NAFLD (2.4 (1.3–7.8) vs. 0.68 (0.05–19.1) U/ml; P = 0.0001) and controls (1.12 (0.01–3.5) U/ml; P = 0.001). FRAP was lower in ALD as compared with NAFLD (345.4 (56–615.9) vs. 434.1 (197.6–733.3) μmol of Fe⁺² liberated; P = 0.001) but similar to that of controls (340.9 (141.5–697.5) μmol of Fe⁺² liberated). Conclusions ALD patients have a higher degree of redox imbalance as compared with NAFLD patients     

瘦素与非酒精性脂肪性肝病的关系

瘦素属于蛋白质激素.主要由白色脂肪组织分泌,由瘦素受体介导发挥生物学作用.最初发现其参与机体代谢调节,控制机体脂肪量.近年来发现其与非酒精性脂肪性肝病的关系密切,但研究结果并不一致.有学者研究发现非酒精性脂肪性肝病患者血清瘦素水平无明显提高,也有学者提出瘦素在非酒精性脂肪性肝病患者中显著提高,并在其发病中具有独立的重要作用,瘦素的抗脂毒性减弱及瘦素抵抗被认为是其中的重要环节.     

瘦素与非酒精性脂肪性肝病的关系

瘦素属于蛋白质激素.主要由白色脂肪组织分泌,由瘦素受体介导发挥生物学作用.最初发现其参与机体代谢调节,控制机体脂肪量.近年来发现其与非酒精性脂肪性肝病的关系密切,但研究结果并不一致.有学者研究发现非酒精性脂肪性肝病患者血清瘦素水平无明显提高,也有学者提出瘦素在非酒精性脂肪性肝病患者中显著提高,并在其发病中具有独立的重要作用,瘦素的抗脂毒性减弱及瘦素抵抗被认为是其中的重要环节.     

瘦素与非酒精性脂肪性肝病的关系

瘦素属于蛋白质激素.主要由白色脂肪组织分泌,由瘦素受体介导发挥生物学作用.最初发现其参与机体代谢调节,控制机体脂肪量.近年来发现其与非酒精性脂肪性肝病的关系密切,但研究结果并不一致.有学者研究发现非酒精性脂肪性肝病患者血清瘦素水平无明显提高,也有学者提出瘦素在非酒精性脂肪性肝病患者中显著提高,并在其发病中具有独立的重要作用,瘦素的抗脂毒性减弱及瘦素抵抗被认为是其中的重要环节.     

糖尿病胰岛移植及细胞治疗的细胞来源

胰岛移植或细胞治疗是根治1型糖尿病较为理想的方法,但同时也面临着供体匮乏的难题。近年来研究显示,除同种自体或异体胰岛外,异种胰岛尤其是选择猪供胰成为众多学者关注的焦点;另外对扩增胰腺β细胞及制造胰岛素分泌细胞株的研究亦取得了一定的成果;而干细胞工程及转基因技术的应用,使利用干细胞治疗糖尿病及人工构建类胰岛细胞成为可能。