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首页> 外文期刊>Chemosphere >Chronic exposure to a pollutant mixture at low doses led to tissue-specific metabolic alterations in male mice fed standard and high-fat high-sucrose diet
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Chronic exposure to a pollutant mixture at low doses led to tissue-specific metabolic alterations in male mice fed standard and high-fat high-sucrose diet

机译:长期低剂量暴露于污染物混合物会导致饲喂标准和高脂高蔗糖饮食的雄性小鼠组织特异性代谢改变

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摘要

Excessive consumption of industrialized food and beverages is a major etiologic factor in the epidemics of obesity and associated metabolic diseases because these products are rich in fat and sugar. In addition, they contain food contact materials and environmental pollutants identified as metabolism disrupting chemicals. To evaluate the metabolic impact of these dietary threats (individually or combined), we used a male mouse model of chronic exposure to a mixture of low-dose archetypal food-contaminating chemicals that was added in standard or high-fat, high-sucrose (HFHS) diet. Specifically, the mixture contained bisphenol A, diethylhexylphthalate, 2,3,7,8-tetrachlorodibenzo-p-dioxine and polychlorinated biphenyl 153. Exposure lasted from 5 to 20 weeks of age. Metabolic exploration was conducted setting the basis of candidate gene expression mRNA analyses in liver, jejunum and adipose tissue depots from 20 week-old mice. Strong metabolic deleterious effects of the HFHS diet were demonstrated in line with obesity-associated metabolic features and insulin resistance. Pollutant exposure resulted in significant changes on plasma triglyceride levels and on the expression levels of genes mainly encoding xenobiotic processing in jejunum; estrogen receptors, regulators of lipoprotein lipase and inflammatory markers in jejunum and adipose tissues as well as adipogenesis markers. Importantly, the impact of pollutants was principally evidenced under standard diet. In addition, depending on nutritional conditions and on the metabolic tissue considered, the impact of pollutants could mimic or oppose the HFHS effects. Collectively, the present study extends the cocktail effect concept of a low-dosed pollutant mixture and originally points to tissue-specificity responsiveness especially in jejunum and adipose tissues. (C) 2019 Elsevier Ltd. All rights reserved.
机译:工业化食品和饮料的过量消费是肥胖症和相关代谢疾病流行病的主要病因,因为这些产品富含脂肪和糖分。此外,它们还包含食品接触材料和被确认为破坏新陈代谢的化学物质的环境污染物。为了评估这些饮食威胁(单独或组合)对代谢的影响,我们使用了雄性小鼠模型,将其长期暴露于低剂量原型食品污染化学物质的混合物中,该混合物已添加到标准或高脂肪,高蔗糖中( HFHS)饮食。具体地,该混合物包含双酚A,邻苯二甲酸二乙基己酯,2,3,7,8-四氯二苯并-对-二恶英和多氯联苯153。暴露持续了5至20周龄。进行了代谢探索,为来自20周龄小鼠的肝脏,空肠和脂肪组织贮库中的候选基因表达mRNA分析奠定了基础。与肥胖相关的代谢特征和胰岛素抵抗一致,证实了HFHS饮食具有强的代谢有害作用。污染物的暴露导致空肠中血浆甘油三酸酯水平和主要编码异源加工过程的基因的表达水平发生显着变化;空肠和脂肪组织中的雌激素受体,脂蛋白脂肪酶的调节剂和炎性标志物以及成脂标志物。重要的是,污染物的影响主要由标准饮食证明。此外,根据营养条件和所考虑的代谢组织,污染物的影响可能会模仿或反对HFHS的影响。总的来说,本研究扩展了低剂量污染物混合物的鸡尾酒效应概念,并最初指出了组织特异性反应性,特别是在空肠和脂肪组织中。 (C)2019 Elsevier Ltd.保留所有权利。

著录项

  • 来源
    《Chemosphere》 |2019年第4期|1187-1199|共13页
  • 作者单位

    Univ Claude Bernard Lyon1, Univ Lyon, INSA Lyon, CarMeN Lab,INSERM U1060,INRA U1397, F-69600 Oullins, France;

    Univ Claude Bernard Lyon1, Univ Lyon, INSA Lyon, CarMeN Lab,INSERM U1060,INRA U1397, F-69600 Oullins, France;

    Univ Claude Bernard Lyon1, Univ Lyon, INSA Lyon, CarMeN Lab,INSERM U1060,INRA U1397, F-69600 Oullins, France;

    Univ Claude Bernard Lyon1, Univ Lyon, INSA Lyon, CarMeN Lab,INSERM U1060,INRA U1397, F-69600 Oullins, France;

    Univ Claude Bernard Lyon1, Univ Lyon, INSA Lyon, CarMeN Lab,INSERM U1060,INRA U1397, F-69600 Oullins, France;

    Univ Claude Bernard Lyon1, Univ Lyon, INSA Lyon, CarMeN Lab,INSERM U1060,INRA U1397, F-69600 Oullins, France;

    Univ Claude Bernard Lyon1, Univ Lyon, INSA Lyon, CarMeN Lab,INSERM U1060,INRA U1397, F-69600 Oullins, France;

    Univ Claude Bernard Lyon1, Univ Lyon, INSA Lyon, CarMeN Lab,INSERM U1060,INRA U1397, F-69600 Oullins, France;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    Mixture of pollutants; Cocktail effect; Endocrine disruptors; High-fat high-sucrose diet; Metabolic disturbances; Obesity;

    机译:污染物混合物;鸡尾酒效应;内分泌干扰物;高脂高蔗糖饮食;代谢紊乱;肥胖;

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