دورية أكاديمية
أعرض في EDS

Mechanism of the development of nonalcoholic steatohepatitis after pancreaticoduodenectomy.

التفاصيل البيبلوغرافية
العنوان: Mechanism of the development of nonalcoholic steatohepatitis after pancreaticoduodenectomy.
المؤلفون: Nagaya T; Department of Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan., Tanaka N; Department of Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan ; Department of Metabolic Regulation, Shinshu University Graduate School of Medicine, Matsumoto, Japan., Kimura T; Department of Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan., Kitabatake H; Department of Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan., Fujimori N; Department of Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan., Komatsu M; Department of Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan., Horiuchi A; Digestive Disease Center, Showa Inan General Hospital, Komagane, Japan., Yamaura T; Department of Gastroenterology, Iida Municipal Hospital, Iida, Japan., Umemura T; Department of Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan., Sano K; Department of Laboratory Medicine, Shinshu University Hospital, Matsumoto, Japan., Gonzalez FJ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, United States., Aoyama T; Department of Metabolic Regulation, Shinshu University Graduate School of Medicine, Matsumoto, Japan., Tanaka E; Department of Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan.
المصدر: BBA clinical [BBA Clin] 2015 Feb 19; Vol. 3, pp. 168-74. Date of Electronic Publication: 2015 Feb 19 (Print Publication: 2015).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: Netherlands NLM ID: 101633879 Publication Model: eCollection Cited Medium: Print ISSN: 2214-6474 (Print) Linking ISSN: 22146474 NLM ISO Abbreviation: BBA Clin Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [Amsterdam] : Elsevier, [2014]-[2017]
مستخلص: Background and Aim: It is recognized that nonalcoholic fatty liver disease (NAFLD), including nonalcoholic steatohepatitis (NASH), may develop after pancreaticoduodenectomy (PD). However, the mechanism of NASH development remains unclear. This study aimed to examine the changes in gene expression associated with NASH occurrence following PD.
Methods: The expression of genes related to fatty acid/triglyceride (FA/TG) metabolism and inflammatory signaling was examined using liver samples obtained from 7 post-PD NASH patients and compared with 6 healthy individuals and 32 conventional NASH patients.
Results: The livers of post-PD NASH patients demonstrated significant up-regulation of the genes encoding CD36, FA-binding proteins 1 and 4, acetyl-coenzyme A carboxylase α, diacylglycerol acyltransferase 2, and peroxisome proliferator-activated receptor (PPAR) γ compared with normal and conventional NASH livers. Although serum apolipoprotein B (ApoB) and TG were decreased in post-PD NASH patients, the mRNAs of ApoB and microsomal TG transfer protein were robustly increased, indicating impaired TG export from the liver as very-low-density lipoprotein (VLDL). Additionally, elevated mRNA levels of myeloid differentiation primary response 88 and superoxide dismutases in post-PD NASH livers suggested significant activation of innate immune response and augmentation of oxidative stress generation.
Conclusions: Enhanced FA uptake into hepatocytes and lipogenesis, up-regulation of PPARγ, and disruption of VLDL excretion into the circulation are possible mechanisms of steatogenesis after PD.
General Significance: These results provide a basis for understanding the pathogenesis of NAFLD/NASH following PD.
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فهرسة مساهمة: Keywords: ACACA, acetyl-CoA carboxylase α; ACACB, acetyl-CoA carboxylase β; ACADM, medium-chain acyl-CoA dehydrogenase; ACOX1, acyl-CoA oxidase 1; ALT, alanine aminotransferase; AST, aspartate aminotransferase; ApoB, apolipoprotein B; BMI, body mass index; CAT, catalase; CPT1A, carnitine palmitoyl-CoA transferase 1α; CT, computed tomography; CYBB, cytochrome b-245 β polypeptide; CYP, cytochrome P450; CoA, coenzyme A; DGAT, diacylglycerol acyltransferase; FA, fatty acid; FABP, fatty acid-binding protein; FASN, fatty acid synthase; Fatty acid; HADHA, hydroxyacyl-CoA dehydrogenase/3-ketoacyl-CoA thiolase/enoyl-CoA hydratase α; HBV, hepatitis B virus; HCV, hepatitis C virus; HOMA-IR, homeostasis model assessment for insulin resistance; LPS, lipopolysaccharide; LXR, liver X receptor; MCD, methionine- and choline-deficient diet; MTTP, microsomal triglyceride transfer protein; MYD88, myeloid differentiation primary response 88; MyD88; NAFLD, nonalcoholic fatty liver disease; NAS, NAFLD activity score; NASH; NASH, nonalcoholic steatohepatitis; PD, pancreaticoduodenectomy; PPAR, peroxisome proliferator-activated receptor; PPARGC, PPARγ co-activator; Pancreaticoduodenectomy; ROS, reactive oxygen species; RXR, retinoid X receptor; SCD, stearoyl-CoA desaturase; SOD, superoxide dismutase; SREBF1, sterol regulatory element-binding transcription factor 1; TG, triglyceride; TGFB1, transforming growth factor β1; TLR, Toll-like receptor; TNF, tumor necrosis factor α; US, ultrasonography; VLDL; VLDL, very-low-density lipoprotein; qPCR, quantitative polymerase chain reaction; γGT, gamma-glutamyltransferase
تواريخ الأحداث: Date Created: 20151218 Date Completed: 20151217 Latest Revision: 20201001
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC4661550
DOI: 10.1016/j.bbacli.2015.02.001
PMID: 26674248
قاعدة البيانات: MEDLINE
الوصف
تدمد:2214-6474
DOI:10.1016/j.bbacli.2015.02.001