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| 1 | Nonalcoholic fatty liver disease as a multi-systemic disease显示文摘Nonalcoholic fatty liver disease(NAFLD) is the most common cause of chronic liver disease. NAFLD includes a wide spectrum of liver conditions ranging from simple steatosis to nonalcoholic steatohepatitis and advanced hepatic fibrosis. NAFLD has been recognized as a hepatic manifestation of metabolic syndrome linked with insulin resistance. NAFLD should be considered not only a liver specific disease but also an early mediator of systemic diseases. Therefore, NAFLD is usually associated with cardiovascular disease, chronic kidney disease, type 2 diabetes, obesity, and dyslipidemia. NAFLD is highly prevalent in the general population and is associated with increased cardiovascular morbidity and mortality. The underlying mechanisms and pathogenesis of NAFLD with regard to other medical disorders are not yet fully understood. This review focuses on pathogenesis of NAFLD and its relation with other systemic diseases. | Hakan Fotbolcu Elcin Zorlu | 2016 | World Journal of Gastroenterology2016，22，16： | 29 |
| 2 | Insulin resistance in development and progression of nonalcoholic fatty liver disease显示文摘Although insulin resistance(IR)is strongly associated with nonalcoholic fatty liver disease(NAFLD),the association of IR and NAFLD is not universal and correlation between IR and severity of NAFLD is still controversial.In this review,we summarize recent evidence that partially dissociates insulin resistance from NAFLD.It has also been reported that single-nucleotide polymorphisms in the diacylglycerol acyltransferase gene,rather than IR,account for the variability in liver fat content.Polymorphisms of the patatin-like phospholipase 3 gene have also been reported to be associated with NAFLD without metabolic syndrome,which suggests that genetic conditions that promote the development of fatty changes in the liver may occur independently of IR.Moreover,environmental factors such as nutrition and physical activity as well as small intestinal bacterial overgrowth have been linked to the pathogenesis of NAFLD,although some of the data are conflicting.Therefore,findings from both genetically engineered animal models and humans with genetic conditions,as well as recent studies that have explored the role of environmental factors,have confirmed the view that NAFLD is a polygenic disease process caused by both genetic and environmental factors.Therefore,IR is not the sole predictor of the pathogenesis of NAFLD. | Shahinul Alam Golam Mustafa Mahabubul Alam Nooruddin Ahmad | 2016 | World Journal of Gastrointestinal Pathophysiology2016，7，2： | 12 |
| 3 | Glycosyltransferases and non-alcoholic fatty liver disease显示文摘Non-alcoholic fatty liver disease(NAFLD) is the most common form of chronic liver disease and its incidence is increasing worldwide. However, the underlying mechanisms leading to the development of NAFLD are still not fully understood. Glycosyltransferases(GTs) are a diverse class of enzymes involved in catalyzing the transfer of one or multiple sugar residues to a wide range of acceptor molecules. GTs mediate a wide range of functions from structure and storage to signaling, and play a key role in many fundamental biological processes. Therefore, it is anticipated that GTs have a role in the pathogenesis of NAFLD. In this article, we present an overview of the basic information on NAFLD, particularly GTs and glycosylation modification of certain molecules and their association with NAFLD pathogenesis. In addition, the effects and mechanisms of some GTs in the development of NAFLD are summarized. | Yu-Tao Zhan Hai-Ying Su Wei An | 2016 | World Journal of Gastroenterology2016，22，8： | 4 |
| 4 | Antifibrotic effects of ambrisentan,an endothelin-A receptor antagonist,in a non-alcoholic steatohepatitis mouse model显示文摘AIM: To examine the effects of the endothelin type A receptor antagonist ambrisentan on hepatic steatosis and fibrosis in a steatohepatitis mouse model.METHODS: Fatty liver shionogi(FLS) FLS-ob/ob mice(male, 12 wk old) received ambrisentan(2.5 mg/kg orally per day; n = 8) or water as a control(n = 5) for 4 wk. Factors were compared between the two groups, including steatosis, fibrosis, inflammation, and endothelin-related gene expression in the liver.RESULTS: In the ambrisentan group, hepatic hydroxyproline content was significantly lower than in the control group(18.0 μg/g ± 6.1 μg/g vs 33.9 μg/g ± 13.5 μg/g liver, respectively, P = 0.014). Hepatic fibrosis estimated by Sirius red staining and areas positive for α-smooth muscle actin, indicative of activated hepatic stellate cells, were also significantly lower in the ambrisentan group(0.46% ± 0.18% vs 1.11% ± 0.28%, respectively, P = 0.0003; and 0.12% ± 0.08% vs 0.25% ± 0.11%, respectively, P = 0.047). Moreover, hepatic RNA expression levels of procollagen-1 and tissue inhibitor of metalloproteinase-1(TIMP-1) were significantly lower by 60% and 45%, respectively, in the ambrisentan group. Inflammation, steatosis, and endothelin-related m RNA expression in the liver were not significantly different between the groups.CONCLUSION: Ambrisentan attenuated the progression of hepatic fibrosis by inhibiting hepatic stellate cell activation and reducing procollagen-1 and TIMP-1 gene expression. Ambrisentan did not affect inflammation or steatosis. | Toshiaki Okamoto Masahiko Koda Kennichi Miyoshi Takumi Onoyama Manabu Kishina Tomomitsu Matono Takaaki Sugihara Keiko Hosho Junichi Okano Hajime Isomoto Yoshikazu Murawaki | 2016 | World Journal of Hepatology2016，8，22： | 0 |
| 5 | Hypolactasia is associated with insulin resistance in nonalcoholic steatohepatitis显示文摘AIM To assess lactase gene(LCT)-13910C>T polymorphisms in Brazilian non-alcoholic fatty liver disease(NAFLD) and nonalcoholic steatohepatitis(NASH) patients in comparison with healthy controls.METHODS This was a transverse observational clinical study with NAFLD patients who were followed at the Hepatology Outpatient Unit of the Hospital das Clínicas, S?o Paulo, Brazil. The polymorphism of lactase non-persistence/lactase persistence(LCT-13910C>T) was examined by PCR-restriction fragment length polymorphism technique in 102 liver biopsy-proven NAFLD patients(steatosis in 9 and NASH in 93) and compared to those of 501 unrelated healthy volunteers. Anthropometric, clinical, biochemical and liver histology data were analyzed. Continuous variables were compared using the t or Mann-Whitney tests, and categorical data were compared with the Fisher's exact test. Univariate logistic regression and multivariate logistic regression adjusted for gender and age were performed.RESULTS No differences in the LCT-13910 genotype frequencies were noted between the NAFLD patients(66.67% of the patients with steatosis were CC, 33.33% were CT, and none were TT; 55.91% of the patients with NASH were CC, 39.78% were CT, and 4.3% were TT; P = 0.941) and the healthy controls(59.12% were CC, 35.67% were CT, and 5.21% were TT) or between the steatosis and NASH patients. That is, the distribution of the lactase non-persistence/lactase persistence polymorphism(LCT-13910C>T) in the patients with NAFLD was equal to that in the general population. In the NASH patients, the univariate analysis revealed that the lactase nonpersistence(low lactase activity or hypolactasia) phenotype was associated with higher insulin levels(23.47 ± 15.94 μU/m L vs 15.8 ± 8.33 μU/m L, P = 0.027) and a higher frequency of insulin resistance(91.84% vs 72.22%, P = 0.02) compared with the lactase persistence phenotype. There were no associations between the LCT genotypes and diabetes(P = 0.651), dyslipidaemia(P = 0.328), hypertension(P = 0.507) or liver histology in these patients. Moreover, in the NASH patients, hypolactasia was an independent risk factor for insulin resistance even after adjusting for gender and age [OR = 5.0(95%CI: 1.35-20; P = 0.017)].CONCLUSION The LCT-13910 genotype distribution in Brazilian NAFLD patients was the same as that of the general population, but hypolactasia increased the risk of insulin resistance in the NASH patients. | Daniel Ferraz de Campos Mazo Rejane Mattar Jose Tadeu Stefano Joyce Matie Kinoshita da Silva-Etto Marcio Augusto Diniz Sebastiao Mauro Bezerra Duarte Fabíola Rabelo Rodrigo Vieira Costa Lima Priscila Brizolla de Campos Flair Jose Carrilho Claudia P Oliveira | 2016 | World Journal of Hepatology2016，8，24： | 0 |
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