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Evaluation of safety for hepatectomy in a novel mouse model with nonalcoholic-steatohepatitis

World Journal of Gastroenterology 2018年第15期24卷 1622-1631页

作者： Yusuke Ozawa Takafumi Tamura Yohei Owada Yoshio Shimizu Akira Kemmochi Katsuji Hisakura Takashi Matsuzaka Hitoshi Shimano Hiroko Isoda Nobuhiro Ohkohchi Department of Gastrointestinal and Hepato-Biliary-Pancreatic Surgery Faculty of Medicine University of Tsukuba Department of Endocrinology and Metabolism Faculty of Medicine University of Tsukuba Faculty of Life and Environmental Sciences University of Tsukuba

AIM To investigate whether the liver resection volume in a newly developed nonalcoholic steatohepatitis(NASH) model influences surgical outcome.METHODS For establishment of a NASH model, mice were fed a high-fat diet for 4 wk, administered CCl_4 for the last 2 wk, and administered T0901317 for the last 5 d. We divided these mice into two groups: A 30% partial hepatectomy(PH) of NASH liver group and a 70% PH of NASH liver group. In addition, a 70% PH of normal liver group served as the control. Each group was evaluated for survival rate, regeneration, apoptosis, necrosis and DNA expression after PH.RESULTS In the 70% PH of NASH group, the survival rate was significantly decreased compared with that in the control and 30% PH of NASH groups(P < 0.01). 10 of 32 mice in the NASH 70% PH group died within 48 h after PH. Serum aspartate aminotransferase(AST) levels and total bilirubin(T-Bil) in the NASH 70% PH group were significantly higher than the levels in the other two groups(AST: P < 0.05, T-Bil: P < 0.01). In both PH of NASH groups, signaling proteins involved in regeneration were expressed at lower levels than those in the control group(P < 0.01). The 70% PH of NASH group also exhibited a lower number of Ki-67-positive cells and higher rates of apoptosis and necrosis than the NASH 30% PH group(P < 0.01). In addition, DNA microarray assays showed differences in gene expression associated with cell cycle arrest and apoptosis.CONCLUSION The function of the residual liver is impaired in fatty liver compared to normal liver. A larger residual volume is required to maintain liver functions in mice with NASH.

关键词： Hepatectomy Liver regeneration Residual liver Liver proliferation nonalcoholic steatohepatitis

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Biomarkers and subtypes of deranged lipid metabolism in nonalcoholic fatty liver disease

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World Journal of Gastroenterology 2019年第24期25卷 3009-3020页

作者： José M Mato Cristina Alonso Mazen Noureddin Shelly C Lu CIC bioGUNE Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (Ciberehd)Technology Park of BizkaiaDerio 48160BizkaiaSpain OWL Metabolomics Technology Park of BizkaiaDerio 48160BizkaiaSpain Division of Digestive and Liver Diseases Comprehensive Transplant CenterCedars-Sinai Medical CenterLos AngelesCA 90048United States

nonalcoholic fatty liver disease(NAFLD)is a heterogeneous and complex disease that is imprecisely diagnosed by liver biopsy.NAFLD covers a spectrum that ranges from simple steatosis,nonalcoholic steatohepatitis(NASH)with varying degrees of fibrosis,to cirrhosis,which is a major risk factor for hepatocellular carcinoma.Lifestyle and eating habit changes during the last century have made NAFLD the most common liver disease linked to obesity,type 2 diabetes mellitus and dyslipidemia,with a global prevalence of 25%.NAFLD arises when the uptake of fatty acids(FA)and triglycerides(TG)from circulation and de novo lipogenesis saturate the rate of FAβ-oxidation and verylow density lipoprotein(VLDL)-TG export.Deranged lipid metabolism is also associated with NAFLD progression from steatosis to NASH,and therefore,alterations in liver and serum lipidomic signatures are good indicators of the disease’s development and progression.This review focuses on the importance of the classification of NAFLD patients into different subtypes,corresponding to the main alteration(s)in the major pathways that regulate FA homeostasis leading,in each case,to the initiation and progression of NASH.This concept also supports the targeted intervention as a key approach to maximize therapeutic efficacy and opens the door to the development of precise NASH treatments.

关键词： S-adenosylmethionine Methionine adenosyltransferase Lipid metabolism Multiomics Lipidomics nonalcoholic steatohepatitis One-carbon metabolism Very low-density lipoproteins Steatosis Precision medicine

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High prevalence of nonalcoholic fatty liver in patients with idiopathic venous thromboembolism

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World Journal of Gastroenterology 2010年第48期16卷 6119-6122页

作者： Matteo Nicola Dario Di Minno Antonella Tufano Anna Rusolillo Giovanni Di Minno Giovanni Tarantino Department of Clinical and Experimental Medicine Federico II University Medical School of Naples

AIM:To assess the prevalence of nonalcoholic fatty liver disease (NAFLD) in patients with idiopathic venous thromboembolism (VTE). METHODS:In a case-control study,after excluding subjects with well-consolidated risk factors for VTE,idiopathic VTE was documented in 138 consecutive patients who were referred to our department. Two hundred and seventy-six healthy sex/age/body-massindex-matched subjects,without any clinical/instrumental evidence of VTE,served as controls. All underwent a clinical/laboratory/ultrasound assessment for the presence of metabolic syndrome and NAFLD. RESULTS:NAFLD was detected in 112/138 cases (81%) and in 84/276 controls (30%) [risk ratio:2.7,95% confidence interval (CI):2.2-3.2,P < 0.0001]. Metabolic syndrome and smoking habit were more prevalent in patients with idiopathic VTE. The high prevalence of NAFLD in VTE was also confirmed after adjustment for inherited thrombophilia. NAFLD was clearly predicted by VTE (odds ratio:1.8,95% CI:1.2-2.7,P < 0.0001).

关键词： Thromboembolism Metabolic syndrome nonalcoholic fatty liver disease

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Diet switch and omega-3 hydroxy-fatty acids display differential hepatoprotective effects in an obesity/nonalcoholic fatty liver disease model in mice

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World Journal of Gastroenterology 2018年第4期24卷 461-474页

作者： Roberto Rodriguez-Echevarria Jose Macias-Barragan Marcela Parra-Vargas Judith Rebeca Davila-Rodriguez Eduardo Amezcua-Galvez Juan Armendariz-Borunda Institute for Molecular Biology and Gene Therapy-CUCS Department of Molecular Biology and GenomicsUniversity of GuadalajaraGuadalajara 44340Mexico Department of Health Sciences-CUValles University of GuadalajaraGuadalajara 46600Mexico Hospital Civil de Guadalajara Guadalajara 46600Mexico

AIM To study the effect of 18-hydroxy-eicosapentaenoic acid(18-HEPE) and 17-hydroxy-docosahexaenoic acid(17-HDHA) in a murine model of obesity/nonalcoholic fatty liver disease.METHODS C57 BL/6 mice were fed with standard chow diet(CD) or high-fat, fructose-enriched diet(HFD) for 16 wk. Then, three groups were treated for 14 d with either, diet switch(HFD for CD), 18-HEPE, or 17-HDHA. Weightand fasting glucose were recorded on a weekly basis. Insulin tolerance test was performed at the end of treatment. Histological analysis(HE and Masson's trichrome stain) and determination of serum insulin, glucagon, glucagon-like peptide 1(GLP-1), glucose-dependent insulinotropic polypeptide, adiponectin and resistin were carried out as well as liver proteins by western blot.RESULTS Mice treated with hydroxy-fatty acids 18-HEPE and 17-HDHA displayed no weight loss or improved insulin sensitivity. However, these mice groups showed a significant amelioration on serum GLP-1, adiponectin and resistin levels. Also, a significant reduction on inflammatory infiltrate was observed at both portal and lobular zones. Furthermore, up-regulation of PPARα/γ protein levels was observed in liver tissue and it was associated with decreased levels of NF-κB also determined by western blot analysis. On the other hand, diet switch regimen resulted in a marked improvement in most parameters including: weight loss, increased insulin sensitivity, decreased steatosis, restored levels of insulin, glucagon, leptin, adiponectin and resistin. However, no significant changes were observed regarding inflammatory infiltrate in this last group.CONCLUSION 18-HEPE and 17-HDHA differentially exert hepatoprotective effects through up-regulation of nuclear receptors PPARα/γ and amelioration of serum adipokines profile.

关键词： nonalcoholic fatty liver disease Polyunsaturated fatty acids 18-hydroxy-eicosapentaenoic acid 17-hydroxy-docosahexaenoic acid Obesity

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PNPLA3 rs139051 is associated with phospholipid metabolite profile and hepatic inflammation in nonalcoholic fatty liver disease

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World Journal of Clinical Cases 2018年第10期6卷 355-364页

作者： Ji-Jun Luo Hai-Xia Cao Rui-Xu Yang Rui-Nan Zhang Qin Pan Department of Gastroenterology Xinhua HospitalShanghai Jiaotong University School of Medicine

AIM To investigate the effect of PNPLA3 polymorphisms on serum lipidomics and pathological characteristics in nonalcoholic fatty liver disease(NAFLD).METHODS Thirty-four biopsy-proven NAFLD patients from Northern, Central, and Southern China were subjected to stratification by genotyping their single nucleotide polymorphisms(SNPs) in PNPLA3. Ultra performance liquid chromatography-tandem mass spectrometry was then employed to characterize the effects of PNPLA3 SNPs on serum lipidomics. In succession, correlation analysis revealed the association of PNPLA3-related lipid profile and hepatic pathological characteristics on a basis of steatosis, activity, and fibrosis assessment. The variant-based scoring of hepatocyte steatosis, ballooning, lobular inflammation, and liver fibrosis was finally performed so as to uncover the actions of lipidomics-affecting PNPLA3 SNPs in NAFLD-specific pathological alterations. RESULTS PNPLA3 SNPs(rs139051, rs738408, rs738409, rs 2072906, rs2294918, rs2294919, and rs4823173) demonstrated extensive association with the serum lipidomics, especially phospholipid metabolites [lysophosphatidylcholine(LPC), lysophosphatidylcholine plasmalogen(LPCO), lysophosphatdylethanolamine(LPE), phosphatidylcholine(PC), choline plasmalogen(PCO), phosphatidylethanolamine(PE), ethanolamine plasmalogen(PEO)], of NAFLD patients. PNPLA3 rs139051(A/A genotype) and rs2294918(G/G genotype) dominated the up-regulatory effect on phospholipids of LPCs(LPC 17:0, LPC 18:0, LPC 20:0, LPC 20:1, LPC 20:2) and LPCOs(LPC O-16:1, LPC O-18:1). Moreover, subjects with high-level LPCs/LPCOs were predisposed to low-grade lobular inflammation of NAFLD(rho:-0.407 to-0.585, P < 0.05-0.001). The significant correlation of PNPLA3 rs139051 and inflammation grading [A/A vs A/G + G/G: 0.50(0.00, 1.75) vs 1.50(1.00, 2.00), P < 0.05] further demonstrated its pathological role based on the modulation of phospholipid metabolite profile.CONCLUSION The A/A genotype at PNPLA3 rs139051 exerts an upregulatory effect on serum phospholipids of

关键词： nonalcoholic fatty liver disease Patatin-like phospholipase domain containing 3 Single nucleotide polymorphism Phospholipid Inflammation

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Role of osteoprotegerin/receptor activator of nuclear factor kappa B/receptor activator of nuclear factor kappa B ligand axis in nonalcoholic fatty liver disease

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World Journal of Gastroenterology 2018年第19期24卷 2073-2082页

作者： Lucia Pacifico Gian Marco Andreoli Miriam D'Avanzo Delia De Mitri Pasquale Pierimarchi Policlinico Umberto I Hospital Sapienza University of Rome Institute of Translational Pharmacology National Research Council

Concomitantly with the increase in the prevalences of overweight/obesity, nonalcoholic fatty liver disease(NAFLD) has worldwide become the main cause of chronic liver disease in both adults and children. Patients with fatty liver display features of metabolic syndrome(Met S), like insulin resistance(IR), glucose intolerance, hypertension and dyslipidemia. Recently, epidemiological studies have linked obesity, Met S, and NAFLD to decreased bone mineral density and osteoporosis, highlighting an intricate interplay among bone, adipose tissue, and liver. Osteoprotegerin(OPG), an important symbol of the receptor activator of nuclear factor-B ligand/receptor activator of nuclear factor kappa B/OPG system activation, typically considered for its role in bone metabolism, may also play critical roles in the initiation and perpetuation of obesityrelated comorbidities. Clinical data have indicated that OPG concentrations are associated with hypertension, left ventricular hypertrophy, vascular calcification, endothelial dysfunction, and severity of liver damage in chronic hepatitis C. Nonetheless, the relationship between circulating OPG and IR as a key feature of Met S as well as between OPG and NAFLD remains uncertain. Thus, the aims of the present review are to provide the existent knowledge on these associations and to discuss briefly the underlying mechanisms linking OPG and NAFLD.

关键词： nonalcoholic fatty liver disease Insulin resistance Metabolic syndrome Osteoprotegerin Receptor activator of nuclear factor kappa B Receptor activator of nuclear factor kappa B ligand

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LB100 ameliorates nonalcoholic fatty liver disease via the AMPK/Sirt1 pathway

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World Journal of Gastroenterology 2019年第45期25卷 6607-6618页

作者： Xue-Yang Chen Chang-Zhou Cai Meng-Li Yu Ze-Min Feng Yu-Wei Zhang Pei-Hao Liu Hang Zeng Chao-Hui Yu Department of Gastroenterology The First Affiliated HospitalCollege of MedicineZhejiang UniversityHangzhou 310003Zhejiang ProvinceChina Clinical Research Center for Hepatobiliary and Pancreatic Diseases of Zhejiang Province Hangzhou 310003Zhejiang ProvinceChina

BACKGROUND It is well known that nonalcoholic fatty liver disease(NAFLD)is associated with insulin resistance(IR).LB100,a serine/threonine protein phosphatase 2A(PP2A)inhibitor,is closely related to IR.However,there is little data regarding its direct influence on NAFLD.AIM To elucidate the effect and underlying mechanism of LB100 in NAFLD.METHODS After 10 wk of high fat diet(HFD)feeding,male C57BL/6 mice were injected intraperitoneally with vehicle or LB100 for an additional 6 wk(three times a week).The L02 cell line was treated with LB100 and free fatty acids(FFAs)for 24 h.Hematoxylin and eosin and oil red O staining were performed for histological examination.Western blot analysis was used to detect the protein expression of Sirtuin 1(Sirt1),total and phosphorylated AMP-activated protein kinaseα(AMPKα),and the proteins involved in lipogenesis and fatty acid oxidation.The mRNA levels were determined by qPCR.Pharmacological inhibition of AMPK was performed to further examine the exact mechanism of LB100 in NAFLD.RESULTS LB100 significantly ameliorated HFD-induced obesity,hepatic lipid accumulation and hepatic injury in mice.In addition,LB100 significantly downregulated the protein levels of acetyl-CoA carboxylase,sterol regulatory element-binding protein 1 and its lipogenesis target genes,including stearoyl-CoA desaturase-1 and fatty acid synthase,and upregulated the levels of proteins involved in fatty acidβ-oxidation,such as peroxisome proliferator-activated receptorα(PPARα),peroxisome proliferator-activated receptor gamma coactivator-1α(PGC-1α),carnitine palmitoyltransferase 1α,acyl-CoA oxidase 1 and uncoupling protein 2,as well as the upstream mediators Sirt1 and AMPKαin the livers of HFD-fed mice.In vitro,LB100 alleviated FFA-induced lipid accumulation in L02 cells through the AMPK/Sirt1 signaling pathway.Further studies showed that the curative effect of LB100 on lipid accumulation was abolished by inhibiting AMPKαin L02 cells.CONCLUSION PP2A inhibition by LB100 significantly ameliorates hepatic steatosis

关键词： LB100 nonalcoholic fatty liver disease Serine/threonine-protein phosphatase 2A Lipid metabolism AMP-activated protein kinaseα Sirtuin 1

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Mouse models for investigating the underlying mechanisms of nonalcoholic steatohepatitis-derived hepatocellular carcinoma

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World Journal of Gastroenterology 2018年第18期24卷 1989-1994页

作者： Kazuki Takakura Tsunekazu Oikawa Yoichi Tomita Yusuke Mizuno Masanori Nakano Chisato Saeki Yuichi Torisu Masayuki Saruta Division of Gastroenterology and Hepatology Department of Internal Medicine The Jikei University School of Medicine

As the incidence of hepatocellular carcinoma(HCC) caused by infection with the hepatotropic viruses hepatitis B and hepatitis C decreases, greater attention has become focused on HCC caused by nonalcoholic steatohepatitis(NASH), an advanced form of nonalcoholic fatty liver disease which has shown increasing prevalence in correspondence with the overall increase in metabolic syndrome over the recent decades. Several clinical population studies have shown a positive relationship between NASH and HCC, while also providing initial insights into the underlying mechanisms of HCC development from NASH. Research into the pathological progression of NASH to HCC has advanced by use of several beneficial rodent models. In this review, we summarize the established mouse models for preclinical research of NASH-associated HCC and discuss the underlying hepatic mechanisms of NASH-related tumorigenesis identified to date that could lead to new targets for treatment and prevention.

关键词： Hepatocellular carcinoma nonalcoholic steatohepatitis nonalcoholic fatty liver disease

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Favorable clinical outcome of nonalcoholic liver cirrhosis patients with coronary artery disease:A population-based study

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World Journal of Gastroenterology 2018年第31期24卷 3547-3555页

作者： Ming-Chang Tsai Tzu-Wei Yang Chi-Chih Wang Yao-Tung Wang Wen-Wei Sung Ming-Hseng Tseng Chun-Che Lin Division of Gastroenterology and Hepatology Department of Internal MedicineChung Shan Medical University HospitalTaichung 402Taiwan Institute of Medicine Chung Shan Medical UniversityTaichung 402Taiwan School of Medicine Chung Shan Medical UniversityTaichung 402Taiwan Institute and Department of Biological Science and Technology National Chiao Tung UniversityHsinchu 300Taiwan Division of Pulmonary Medicine Chung Shan Medical University HospitalTaichung 402Taiwan Department of Urology Chung Shan Medical University HospitalTaichung 402Taiwan Department of Medical Informatics Chung Shan Medical UniversityTaichung 402Taiwan

AIM To elucidate the prevalence and risk of mortality of nonalcoholic liver cirrhosis(LC) patients with coronary artery disease(CAD).METHODS The study cohort included newly diagnosed nonalcoholic LC patients age ≥ 40 years old without a diagnosis of CAD from 2006 until 2011 from a longitudinal health insurance database. The mean follow-up period for the study cohort was 1152 ± 633 d. The control cohort was matched by sex, age, residence, and index date. Hazard ratios(HRs) were calculated using the Cox proportional hazard model and the Kaplan-Meier method. RESULTS After exclusion, a total of 3409 newly diagnosed nonalcoholic cirrhotic patients were identified from one million samples from the health insurance database. We found that CAD(5.1% vs 17.4%) and hyperlipidemia(20.6% vs 24.1%) were less prevalent in nonalcoholic LC patients than in normal subjects(all P nonalcoholic cirrhotic patients(AHR = 2.34; 95%CI: 2.06-2.65, P nonalcoholic LC. The AHR of CAD in nonalcoholic LC patients was 0.56(95%CI: 0.43-0.74, P nonalcoholic LC patients with and without CAD were 52% and 50%, respectively(P = 0.012). CONCLUSION We conclude that CAD was less prevalent and associated with a reduced risk of mortality in nonalcoholic cirrhotic patients.

关键词： nonalcoholic liver cirrhosis Coronary artery disease Population-based study

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Allyl isothiocyanate ameliorates lipid accumulation and inflammation in nonalcoholic fatty liver disease via the Sirt1/AMPK and NF-κB signaling pathways

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World Journal of Gastroenterology 2019年第34期25卷 5120-5133页

作者： Chun-Xiao Li Jian-Guo Gao Xing-Yong Wan Yi Chen Cheng-Fu Xu Ze-Min Feng Hang Zeng Yi-Ming Lin Han Ma Ping Xu Chao-Hui Yu You-Ming Li Department of Gastroenterology the First Affiliated HospitalCollege of MedicineZhejiang UniversityHangzhou 310003Zhejiang ProvinceChina Clinical Research Center for Hepatobiliary and Pancreatic Diseases of Zhejiang Province Hangzhou 310003Zhejiang ProvinceChina

BACKGROUND Allyl isothiocyanate(AITC),a classic anti-inflammatory and antitumorigenic agent,was recently identified as a potential treatment for obesity and insulin resistance.However,little is known about its direct impact on the liver.AIM To investigate the effect and underlying mechanism of AITC in nonalcoholic fatty liver disease(commonly referred to as NAFLD).METHODS To establish a mouse and cellular model of NAFLD,C57BL/6 mice were fed a high fat diet(HFD)for 8 wk,and AML-12 cells were treated with 200μM palmitate acid for 24 h.For AITC treatment,mice were administered AITC(100 mg/kg/d)orally and AML-12 cells were treated with AITC(20μmol/L).RESULTS AITC significantly ameliorated HFD-induced weight gain,hepatic lipid accumulation and inflammation in vivo.Furthermore,serum alanine aminotransferase and aspartate aminotransferase levels were markedly reduced in AITC-treated mice.Mechanistically,AITC significantly downregulated the protein levels of sterol regulatory elementbinding protein 1(SREBP1)and its lipogenesis target genes and upregulated the levels of proteins involved in fatty acidβ-oxidation,as well as the upstream mediators Sirtuin 1(Sirt1)and AMPactivated protein kinaseα(AMPKα),in the livers of HFD-fed mice.AITC also attenuated the nuclear factor kappa B(NF-κB)signaling pathway.Consistently,AITC relieved palmitate acid-induced lipid accumulation and inflammation in AML-12 cells in vitro through the Sirt1/AMPK and NF-κB signaling pathways.Importantly,further studies showed that the curative effect of AITC on lipid accumulation was abolished by siRNA-mediated knockdown of either Sirt1 or AMPKαin AML-12 cells.CONCLUSION AITC significantly ameliorates hepatic steatosis and inflammation by activating the Sirt1/AMPK pathway and inhibiting the NF-κB pathway.Therefore,AITC is a potential therapeutic agent for NAFLD.

关键词： Allyl isothiocyanate nonalcoholic fatty liver disease Hepatic steatosis Liver inflammation

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