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Liver macrophages mediate effects of downhill running and caloric restriction on nonalcoholic fatty liver disease of high fat diet-fed mice.

肝巨噬细胞介导下坡跑和热量限制对高脂饮食喂养小鼠非酒精性脂肪肝的影响。

  • 影响因子:3.40
  • DOI:10.1016/j.lfs.2020.117978
  • 作者列表:"Ai L","Luo W","Yuan P","Liu L","Zhou Y
  • 发表时间:2020-06-15
Abstract

AIMS:The mechanism of physical activity and calorie restriction remedying non-alcoholic fatty liver disease (NAFLD) remains elusive. The purpose of this study is to explore the effects of eccentric exercise and dietary regulation allied or alone on high-fat diet (HFD) induced NAFLD and its potential mechanism. MATERIALS AND METHODS:Mice were fed with HFD for 12 weeks and subsequently treated with chronic downhill running and caloric restriction for 8 weeks. Related biochemical index were examined both before and during intervention to evaluate the liver injury and dyslipidemia. Levels of MCP1, TNFα, IL-1β, IL-6 and IL-10 were detected by ELISA. Liver morphology was observed by H&E and oil red O staining. Protein contents of iNOS, Arg-1, IL-1β and IL-10 were determined by Western blot. CD86 and CD206 fluorescence were determined by Immunofluorescence. KEY FINDING: (1) 12 weeks' HFD induced hyperlipemia and hepatic steatosis by activating M1 macrophages phenotype and inhibiting M2 macrophages. (2) Chronic downhill running and caloric restriction promoted liver M2 macrophages phenotype, and inhibited M1 macrophages, to attenuate chronic inflammation and ameliorate hepatic steatosis. (3) The effects of downhill running and dietary regulation allied were more effective on improving NAFLD compared with downhill running or caloric restriction alone. SIGNIFICANCE:Eccentric exercise accompanied by caloric restriction attenuates HFD-related NAFLD by promoting M2 macrophages phenotype and inhibiting M1 macrophages in liver. These findings may be help to designing better non-pharmacological intervention programs for NAFLD patients.

摘要

目的: 体力活动和热量限制治疗非酒精性脂肪性肝病 (NAFLD) 的机制仍不清楚。本研究旨在探讨离心运动和饮食调节联合或单独对高脂饮食 (HFD) 诱导的 NAFLD 的影响及其潜在机制。 材料和方法: 用 HFD 喂养小鼠 12 周,随后用慢性下坡跑和热量限制治疗 8 周。干预前及干预过程中检测相关生化指标,评价肝损伤及血脂异常。ELISA 法检测 MCP1 、 tnf α 、 il-1 β 、 IL-6 、 IL-10 水平。通过 H & E 和油红 O 染色观察肝脏形态。Western blot 法测定 iNOS 、 Arg-1 、 il-1 β 和 IL-10 的蛋白含量。免疫荧光法测定 CD86 和 CD206 荧光。关键发现 :( 1) 12 周的 HFD 通过激活 M1 巨噬细胞表型和抑制 M2 巨噬细胞诱导高脂血症和肝脏脂肪变性。(2) 慢性下坡跑和热量限制可促进肝 M2 巨噬细胞表型,抑制 M1 巨噬细胞,减轻慢性炎症,改善肝脏脂肪变性。(3) 与单纯下坡跑或热量限制相比,下坡跑和饮食调节联合作用对改善 NAFLD 更有效。 意义: 伴有热量限制的离心运动通过促进肝脏 M2 巨噬细胞表型和抑制 M1 巨噬细胞来减弱 HFD 相关的 NAFLD。这些发现可能有助于为 NAFLD 患者设计更好的非药物干预方案。

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翻译标题与摘要 下载文献
影响因子:3.87
发表时间:2020-02-01
DOI:10.1111/liv.14321
作者列表:["Chen VL","Chen Y","Du X","Handelman SK","Speliotes EK"]

METHODS:BACKGROUND AND AIMS:Cirrhosis is characterized by extensive fibrosis of the liver and is a major cause of liver-related mortality. Cirrhosis is partially heritable but genetic contributions to cirrhosis have not been systemically explored. Here, we carry out association analyses with cirrhosis in two large biobanks and determine the effects of cirrhosis associated variants on multiple human disease/traits. METHODS:We carried out a genome-wide association analysis of cirrhosis as a diagnosis in UK BioBank (UKBB; 1088 cases vs. 407 873 controls) and then tested top-associating loci for replication with cirrhosis in a hospital-based cohort from the Michigan Genomics Initiative (MGI; 875 cases of cirrhosis vs. 30 346 controls). For replicating variants or variants previously associated with cirrhosis that also affected cirrhosis in UKBB or MGI, we determined single nucleotide polymorphism effects on all other diagnoses in UKBB (PheWAS), common metabolic traits/diseases and serum/plasma metabolites. RESULTS:Unbiased genome-wide association study identified variants in/near PNPLA3 and HFE, and candidate variant analysis identified variants in/near TM6SF2, MBOAT7, SERPINA1, HSD17B13, STAT4 and IFNL4 that reproducibly affected cirrhosis. Most affected liver enzyme concentrations and/or aspartate transaminase-to-platelet ratio index. PheWAS, metabolic trait and serum/plasma metabolite association analyses revealed effects of these variants on lipid, inflammatory and other processes including new effects on many human diseases and traits. CONCLUSIONS:We identified eight loci that reproducibly associate with population-based cirrhosis and define their diverse effects on human diseases and traits.

翻译标题与摘要 下载文献
影响因子:2.57
发表时间:2020-02-01
DOI:10.1111/eci.13198
作者列表:["Li H","Wieser A","Zhang J","Liss I","Markwardt D","Hornung R","Neumann-Cip AC","Mayerle J","Gerbes A","Steib CJ"]

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