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首页> 外文期刊>The Journal of Nutritional Biochemistry >Alterations to the microbiota-colon-brain axis in high-fat-diet-induced obese mice compared to diet-resistant mice
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Alterations to the microbiota-colon-brain axis in high-fat-diet-induced obese mice compared to diet-resistant mice

机译：与耐食小鼠相比，高脂肪饮食诱导的肥胖小鼠的微生物肿瘤脑轴的改变

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摘要

Obesity is underpinned by both genetic and environmental factors, including a high-saturated-fat diet. Some mice develop diet-induced obesity (DIO), but others remain diet resistant (DR) despite intake of the same high-saturated-fat diet, a phenomenon that mimics characteristics of the human obese phenotype. Microbiota-colon-brain axis regulation is important for energy metabolism and cognition. Using DIO and DR mouse models, this study aimed to examine gut microbiota, colonic inflammation and cognitive function to elucidate the role of microbiota-gut-brain regulation in DIO. C57B16/J mice fed a chronic saturated-palmitic-acid diet for 22 weeks showed significant body weight gain differences, with the top one third gaining 48% heavier body weight than the lower one third. There was significant reduction in gut microbiota richness and diversity in DIO mice but not in DR mice. At the phylum level, DIO mice had increased abundance of Firmicutes and Antinobacteria, and decreased abundance of Bacterioides and Proteobacteria in gut microbiota. DIO mice exhibited reduced tight junction proteins, increased plasma endotoxin lipopolysaccharide (LPS) and increased inflammation in the colon and liver. Recognition memory and spatial memory were impaired in DIO mice, associated with decreased Bacteroidetes. Further examination showed that hippocampal brain-derived neurotrophic factor was significantly decreased in DIO mice (vs. DR). Conversely, DR mice showed no changes in the above parameters measured. Therefore, gut microbiota, colon inflammation and circulating LPS may play a major role in the development of the obese phenotype and cognitive decline associated with a chronic high-saturated-palmitic-acid diet. (C) 2018 Published by Elsevier Inc.
机译：肥胖是由遗传和环境因素的基础，包括高饱和脂肪的饮食。一些小鼠培养饮食诱导的肥胖症（DIO），但尽管摄入相同的高饱和脂肪饮食，但其他小鼠仍保持饮食（DR），这是一种模仿人体肥胖表型的特征的现象。 Microbiota-colon-脑轴调节对于能量代谢和认知是重要的。本研究采用DIO和博士模型，旨在检查肠道微生物群，结肠癌炎症和认知功能，以阐明微生物肿瘤脑调控在DIO中的作用。 C57B16 / J小鼠喂养慢性饱和棕榈酸饮食22周显示出显着的体重增加差异，顶部三分之一的体重比下降48％更高的体重。在DIO小鼠中肠道微生物群丰富性和多样性显着降低，但在小鼠博士中没有。在门水平，DIO小鼠的丰富性和抗胰腺癌越来越丰富，降低了肠道微生物菌的杀菌剂和噬菌体丰富。 DIO小鼠表现出较小的紧密结蛋白，增加血浆内毒素脂多糖（LPS）和结肠和肝脏的炎症增加。在DIO小鼠中识别识别记忆和空间记忆损害，与细胞减少相关。进一步检查表明，DIO小鼠（VS.DR）中，海马脑衍生的神经营养因子显着降低。相反，小鼠博士没有测量上述参数的变化。因此，肠道微生物，结肠炎症和循环LPS可能在肥胖表型和与慢性高饱和棕榈酸饮食相关的肥胖表型和认知下降的发展中发挥重要作用。 （c）2018年由elsevier公司发布

著录项

  • 来源
    《The Journal of Nutritional Biochemistry》 |2019年第2019期|共12页
  • 作者

    Zhang Peng; Yu Yinghua; Qin Yanfang; Zhou Yuan; Tang Renxian; Wang Qingling; Li Xiangyang; Wang Hongqin; Weston-Green Katrina; Huang Xu-Feng; Zheng Kuiyang;

  • 作者单位

    Xuzhou Med Univ Dept Pathogen Biol &

    Immunol Xuzhou 221004 Jiangsu Peoples R China;

    Xuzhou Med Univ Dept Pathogen Biol &

    Immunol Xuzhou 221004 Jiangsu Peoples R China;

    Xuzhou Med Univ Dept Pathogen Biol &

    Immunol Xuzhou 221004 Jiangsu Peoples R China;

    Xuzhou Med Univ Dept Pathogen Biol &

    Immunol Xuzhou 221004 Jiangsu Peoples R China;

    Xuzhou Med Univ Dept Pathogen Biol &

    Immunol Xuzhou 221004 Jiangsu Peoples R China;

    Xuzhou Med Univ Dept Pathogen Biol &

    Immunol Xuzhou 221004 Jiangsu Peoples R China;

    Xuzhou Med Univ Dept Pathogen Biol &

    Immunol Xuzhou 221004 Jiangsu Peoples R China;

    Univ Wollongong Sch Med Northfields Ave Wollongong NSW 2522 Australia;

    Univ Wollongong Sch Med Northfields Ave Wollongong NSW 2522 Australia;

    Xuzhou Med Univ Dept Pathogen Biol &

    Immunol Xuzhou 221004 Jiangsu Peoples R China;

    Xuzhou Med Univ Dept Pathogen Biol &

    Immunol Xuzhou 221004 Jiangsu Peoples R China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生物化学;
  • 关键词

    Palmitic acid diet; Obesity; Gut microbiota; Colonic inflammation; Cognition; BDNF;

    机译：棕榈酸饮食;肥胖;肠道微生物肿;结肠炎症;认知;BDNF;

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