Fish oil fed prior to ethanol administration prevents acute ethanol-induced fatty liver in mice
Fish oil fed prior to ethanol administration prevents acute ethanol-induced fatty liver in mice
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DOI：
10.1016/j.jhep.2008.04.026
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发表时间：
2008-09-01
影响因子：
25.7
通讯作者：
Ezaki, Osamu
中科院分区：
文献类型：
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作者：
Wada, Satoshi;Yamazaki, Tomomi;Ezaki, Osamu
背景/目标：我们研究了膳食鱼油是否可以防止急性乙醇（酒精）诱导的fatty liver.Methods：小鼠饲喂红花油，鱼油，或红花油加上一个过氧化物酶体增殖物激活物激活物α（PPAR α）的前一天，乙醇管理。油红O染色、血清分析和RT-PCR用于分析乙醇诱导的脂肪肝。结果：在喂食红花油的小鼠中，乙醇使肝脏TG增加3倍，并激活SREBP-1c和ChREBP，促进脂肪生成，增加PPAR γ和DGATs mRNA的表达，促进TG合成。当小鼠被喂食鱼油时，乙醇诱导的脂肪肝减少了73%。鱼油降低了SREBP-1c活性，增加了PPARa活性。然而，在喂食鱼油的小鼠中，响应于乙醇，DGAT 1、DGAT 2、ChREBP、LPK和PPAR γ mRNA的水平增加。预先给予PPAR α激活剂Wy 14643不能抑制乙醇诱导的脂肪肝，提示PPAR α在预防鱼油引起的乙醇诱导的脂肪肝中作用不大。然而，预先摄入鱼油至少部分地通过降低基础SREBP-1c活性，特别是SCD 1的显著降低。(C)2008年欧洲肝脏研究协会。Elsevier B. V.出版，保留所有权利。
Background/Aims: We examined whether dietary fish oil can prevent acute ethanol (alcohol)-induced fatty liver.Methods: Mice were fed safflower oil, fish oil, or safflower oil plus a PPAR alpha activator on the day prior to ethanol administration. Oil red O staining, serum analysis, and RT-PCR were used to analyze ethanol-induced fatty liver.Results: In mice fed safflower oil, ethanol increased liver TG 3-fold, with activation of SREBP-1c and ChREBP, which promote de novo lipogenesis, and increases in expression of mRNAs for PPAR gamma and DGATs mRNAs, which promote TG synthesis. When mice were fed fish oil, ethanol-induced fatty liver was reduced by 73%. Fish oil decreased SREBP-1c activity and increased PPARa activity. However, levels of DGAT1, DGAT2, ChREBP, LPK, and PPAR gamma mRNAs were increased in response to ethanol in mice fed fish oil. Prior administration of Wy14643, PPAR alpha activator, did not inhibit ethanol-induced fatty liver, suggesting that PPAR alpha played little role in prevention of ethanol-induced fatty liver by fish oil.Conclusions: A single dose of ethanol increases the liver TG level via several mechanisms; however, prior ingestion of fish oil effectively prevents ethanol-induced fatty liver, at least in part, by decreasing basal SREBP-1c activity, especially a marked reduction in SCD1. (C) 2008 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.