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首页> 外文期刊>Lipids >Dietary trans-Fatty Acid Induced NASH is Normalized Following Loss of trans-Fatty Acids from Hepatic Lipid Pools
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Dietary trans-Fatty Acid Induced NASH is Normalized Following Loss of trans-Fatty Acids from Hepatic Lipid Pools

机译：肝脂质池中反式脂肪酸的损失使饮食中反式脂肪酸诱导的NASH正常化

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摘要

Previous experiments in mice showed that dietary trans-fats could play a role in non-alcoholic steatohepatitis (NASH) yet little is known about the accumulation trans-fats in hepatic lipid pools in relationship to liver injury. NASH is also associated with obesity yet improves with only modest weight loss. To distinguish the role of obesity versus sustained consumption of a trans-fat containing diet in causing NASH, mice with obesity and NASH induced by consuming a high trans-fat diet for 16 weeks were subsequently fed standard chow or maintained on trans-fat chow for another 8 weeks. The accumulation, partitioning and loss of trans-fats in the major hepatic lipid pools during and after trans-fat consumption were determined. Obese mice switched to standard chow remained obese but steatohepatitis improved. trans-fats were differentially incorporated into the major hepatic lipid pools and the loss of trans-fats after crossover to control chow was greatest in the cholesteryl ester pool. In summary, dietary changes can improve the biochemical and histopathological changes of NASH despite persistent obesity in mice. Analysis of hepatic lipids confirmed that dietary trans-fats accumulate in the major lipid pools and are released differentially with diet normalization. The substantial loss of trans-fats from the cholesteryl ester pool in parallel with improvement in NASH suggests that this pool of trans-fats could play a role in the pathogenesis of NASH.
机译：先前在小鼠中进行的实验表明，饮食中的反式脂肪可能在非酒精性脂肪性肝炎（NASH）中起作用，但对与肝脏损伤相关的肝脂质池中反式脂肪的累积知之甚少。 NASH也与肥胖有关，但仅通过适度的体重减轻即可改善。为了区分肥胖与持续摄入含反式脂肪的饮食在引起NASH中的作用，通过高脂饮食连续16周对肥胖和NASH小鼠进行标准喂养或维持其高脂饮食。再过8周。确定了反式脂肪消耗过程中和摄入后主要肝脏脂质库中反式脂肪的积累，分配和损失。改用标准饲料的肥胖小鼠仍然肥胖，但脂肪性肝炎有所改善。反式脂肪被差异地结合到主要的肝脂质库中，在控制胆固醇的交换之后，反式脂肪的损失在胆固醇酯库中最大。总之，尽管小鼠持续肥胖，但饮食变化仍可以改善NASH的生化和组织病理学变化。肝脂质的分析证实，饮食中的反式脂肪会在主要的脂质库中积累，并随着饮食正常化而有差异地释放。胆固醇酯库中反式脂肪的大量损失与NASH的改善同时显示，这一系列反式脂肪可能在NASH的发病机理中起作用。

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  • 来源
    《Lipids》 |2012年第10期|p.941-950|共10页
  • 作者

    Brent A. Neuschwander-Tetri; David A. Ford; Sahaja Acharya; George Gilkey; Metin Basaranoglu; Laura H. Tetri; Elizabeth M. Brunt;

  • 作者单位

    Division of Gastroenterology and Hepatology, Department of Internal Medicine, Saint Louis University, Saint Louis, USA;

    Department of Biochemistry and Molecular Biology, Saint Louis University, Saint Louis, USA;

    School of Medicine, Saint Louis University, Saint Louis, USA;

    School of Medicine, Saint Louis University, Saint Louis, USA;

    Division of Gastroenterology and Hepatology, Department of Internal Medicine, Saint Louis University, Saint Louis, USA;

    Division of Gastroenterology and Hepatology, Department of Internal Medicine, Saint Louis University, Saint Louis, USA;

    Department of Pathology and Immunology, Washington University, Saint Louis, USA;

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  • 正文语种 eng
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  • 关键词

    High fructose corn syrup; Fatty liver; Obesity; Leptin; Resistin;

    机译：高果糖玉米糖浆;脂肪肝;肥胖症;瘦素;抵抗素;

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