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| 1 | Genetic factors that affect nonalcoholic fatty liver disease: A systematic clinical review显示文摘AIM: To investigate roles of genetic polymorphisms in non-alcoholic fatty liver disease(NAFLD) onset, severity, and outcome through systematic literature review. METHODS: The authors conducted both systematic and specific searches of Pub Med through December 2015 with special emphasis on more recent data(from 2012 onward) while still drawing from more historical data for background. We identified several specific genetic polymorphisms that have been most researched and, at this time, appear to have the greatest clinical significance on NAFLD and similar hepatic diseases. These were further investigated to assess their specific effects on disease onset and progression and the mechanisms by which these effects occur. RESULTS: We focus particularly on genetic polymorphisms of the following genes: PNPLA3, particularly the p. I148 M variant, TM6SF2, particularly the p. E167 K variant, and on variants in FTO, LIPA, IFNλ4, and iron metabolism, specifically focusing on HFE, and HMOX-1. We discuss the effect of these genetic variations and their resultant protein variants on the onset of fatty liver disease and its severity, including the effect on likelihood of progression to cirrhosis and hepatocellular carcinoma. While our principal focus is on NAFLD, we also discuss briefly effects of some of the variants on development and severity of other hepatic diseases, including hepatitis C and alcoholic liver disease. These results are briefly discussed in terms of clinical application and future potential for personalized medicine. CONCLUSION: Polymorphisms and genetic factors of several genes contribute to NAFLD and its end results. These genes hold keys to future improvements in diagnosis and management. | Tyler J Severson Siddesh Besur Herbert L Bonkovsky | 2016 | World Journal of Gastroenterology2016，22，29： | 12 |
| 2 | Lipidomics as a Principal Tool for Advancing Biomedical Research显示文摘Lipidomics,在 lipidome 的一张全面地图的构造指向在一个房间或纸巾以内包括全部类脂化合物水池,当前在类脂化合物生物学,技术和药的接口作为一个独立学科正在出现。生物 lipidomes 的差异和复杂性打电话让技术革新和改进满足各种各样的生物医学的研究的需要。特别地, lipidomic 研究的领域里的扩大的最近的波浪主要在分析技术被归因于进展为在细胞的 lipidome 的多样的类脂化合物种类的宽数组的描述和 quantification 的新集体度谱、色析法的工具的开发。这里,我们在 lipidome 分析考察一些关键技术进展并且向前把 lipidomics 的应用放在包括新陈代谢的症候群, neurodegenerative 疾病和传染疾病在众多的疾病模型探讨类脂化合物的生物角色,为为生物医学的研究有用的各种各样的 mammalian/organism 模型象增加的紧急一样盘点构造 lipidome 。 | Sin Man Lam Guanghou Shui | 2013 | Journal of Genetics and Genomics2013，40，8： | 10 |
| 3 | The Involvement of Lipids in Alzheimer's Disease显示文摘It has been estimated that Alzheimer's disease(AD), the most common form of dementia, will affect approximately 81 million individuals by 2040. To date, the actual cause and cascade of events in the progression of this disease have not been fully determined.Furthermore, there is currently no definitive blood test or simple diagnostic method for AD. Considerable efforts have been put into proteomic approaches to develop a diagnostic blood test, but to date these efforts have not been successful. More recently, there has been a stronger focus on lipidomic studies in the hope of increasing our understanding of the underlying mechanisms leading to AD and developing an AD blood test. It is well known that the strongest genetic risk factor for AD is the ε4 variant of apolipoprotein E(APOE).Evidence suggests that the ApoE protein, a major lipid transporter, plays a key role in the pathogenesis of AD, and its role in both normal and aberrant lipid metabolism warrants further extensive investigation. Here, we review ApoE-lipid interactions, as well as the roles that lipids may play in the pathogenesis of AD. | Wei Ling Florence Lim Ian James Martins Ralph Nigel Martins | 2014 | Journal of Genetics and Genomics2014，41，5： | 6 |
| 4 | Fatty liver in childhood显示文摘Fatty liver is a growing health problem worldwide. It might evolve to nonalcoholic steatohepatitis, cirrhosis and cause hepatocellular carcinoma. This disease, which has increased because of eating habits, changes in food content and lifestyle, affects people from childhood. The most important risk factors are obesity and insulin resistance. Besides these factors, gender, ethnicity, genetic predisposition and some medical problems are also important. Cirrhosis in children is rare but is reported. Nonalcoholic fatty liver disease(NAFLD) has no specific symptoms or signs but should be considered in obese children. NAFLD does not have a proven treatment. Weight loss with family based treatments is the most acceptable management. Exercise and an applicable diet with low glycemic index and appropriate calorie intake are preferred. Drugs are promising but not sufficient in children for today. | Yesim Ozturk Ozlem Bekem Soylu | 2014 | World Journal of Hepatology2014，6，1： | 3 |
| 5 | 高血糖对非酒精性脂肪性肝炎大鼠肝星状细胞活化作用的研究显示文摘目的观察高血糖在非酒精性脂肪性肝炎(NASH)、肝纤维化形成中的作用以及此过程中肝星状细胞的活化机制。方法将60只SD大鼠分威正常对照组、高血糖模型组、复合模型组、氨基胍组和格列美脲组5组,分别检测各组大鼠血糖值,HE染色观察肝组织的病理改变,Masson染色观察肝脏纤维组织变化,免疫组化检测α-平滑肌动蛋白(α-SMA)的表达评分、ELISA法检测基质金属蛋白酶组织抑制因子-1(TIMP-1)、转化生长因子-β1(TGF-β1)和晚期糖基化终产物(AGEs)含量的变化。结果氨基胍组、格列美脲组大鼠的血糖值较高血糖模型组和复合模型组均降低(均P<0.05);光镜下观察高血糖模型组和复合模型组出现肝细胞变性和纤维化改变。与复合模型组比较,格列美脲组肝细胞形态较正常,可见轻度水肿、脂肪变性及炎细胞浸润,纤维化明显降低,α-SMA表达明显降低,TIMP-1、TGF-β1、AGEs含量也显著降低,均有统计学差异(均P<0.01)。与复合模型组比较,氨基胍组肝组织形态明显改善,脂肪变性、水样变性、纤维化程度有所减轻,TIMP-1、AGEs含量降低(均P<0.01),α-SMA表达增高(P<0.05),同时TGF-β1表达减低,但无统计学差异(P>0.05)。结论高血糖促进了NASH、肝纤维化的形成,通过降低血糖和减少AGEs形成后,肝纤维化程度也有所减轻;机制之一是激活肝星状细胞。格列美脲较氨基胍改善NASH、肝纤维化更明显。 | 杜卫东 夏超 项标 李俊杰 施军平 | 2014 | 浙江医学2014，36，8： | 2 |
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