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Artificial sweeteners induce glucose intolerance by altering the gut microbiota

机译：人造甜味剂通过改变肠道菌群诱导葡萄糖耐受不良

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摘要

我们使用不含热量的人造甜味剂已经超过一个世纪了。今天食品工业将它们用在食品中的数量越来越大，同时它们也被推荐用于减肥和供患葡萄糖耐受不良及2-型糖尿病的人使用。Eran Elinav及同事发现，三种最常用的不含热量的人造甜味剂（糖精、三氯蔗糖和阿斯巴甜）的消耗，会直接诱发小鼠产生肥胖和葡萄糖耐受不良倾向。这些效应由小肠微生物群的组成和功能的变化调节，有害代谢效应可以通过"粪便移植"转移给无菌小鼠，并可通过抗生素治疗被消除。作者显示，人造甜味剂能诱发健康人士发生菌群失调和葡萄糖耐受不良。他们提出，可能有必要制定专门针对个体以及针对肠道微生物群变化的新的营养策略。%Non-caloric artificial sweeteners (NAS) are among the most widely used food additives worldwide, regularly consumed by lean and obese individuals alike. NAS consumption is considered safe and beneficial owing to their low caloric content, yet supporting scientific data remain sparse and controversial. Here we demonstrate that consumption of commonly used NAS formulations drives the development of glucose intolerance through induction of compositional and functional alterations to the intestinal microbiota. These NAS-mediated deleterious metabolic effects are abrogated by antibiotic treatment, and are fully transferable to germ-free mice upon faecal transplantation of microbiota configurations from NAS - consuming mice, or of microbiota anaerobically incubated in the presence of NAS. We identify NAS-altered microbial metabolic pathways that are linked to host susceptibility to metabolic disease, and demonstrate similar NAS-induced dysbiosis and glucose intolerance in healthy human subjects. Collectively, our results link NAS consumption, dysbiosis and metabolic abnormalities, thereby calling for a reassessment of massive NAS usage.
机译：我们使用不含热量的人造甜味剂已经超过一个世纪了。今天食品工业将它们用在食品中的数量越来越大，同时它们也被推荐用于减肥和供患葡萄糖耐受不良及2-型糖尿病的人使用。Eran Elinav及同事发现，三种最常用的不含热量的人造甜味剂（糖精、三氯蔗糖和阿斯巴甜）的消耗，会直接诱发小鼠产生肥胖和葡萄糖耐受不良倾向。这些效应由小肠微生物群的组成和功能的变化调节，有害代谢效应可以通过"粪便移植"转移给无菌小鼠，并可通过抗生素治疗被消除。作者显示，人造甜味剂能诱发健康人士发生菌群失调和葡萄糖耐受不良。他们提出，可能有必要制定专门针对个体以及针对肠道微生物群变化的新的营养策略。%Non-caloric artificial sweeteners (NAS) are among the most widely used food additives worldwide, regularly consumed by lean and obese individuals alike. NAS consumption is considered safe and beneficial owing to their low caloric content, yet supporting scientific data remain sparse and controversial. Here we demonstrate that consumption of commonly used NAS formulations drives the development of glucose intolerance through induction of compositional and functional alterations to the intestinal microbiota. These NAS-mediated deleterious metabolic effects are abrogated by antibiotic treatment, and are fully transferable to germ-free mice upon faecal transplantation of microbiota configurations from NAS - consuming mice, or of microbiota anaerobically incubated in the presence of NAS. We identify NAS-altered microbial metabolic pathways that are linked to host susceptibility to metabolic disease, and demonstrate similar NAS-induced dysbiosis and glucose intolerance in healthy human subjects. Collectively, our results link NAS consumption, dysbiosis and metabolic abnormalities, thereby calling for a reassessment of massive NAS usage.

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  • 来源
    《Nature》 |2014年第7521期|181-186a1|共7页
  • 作者

    Jotham Suez; Tal Korem; David Zeevi; Gili Zilberman-Schapira1; Christoph A. Thaiss; Ori Maza; David Israeli; Niv Zmora; Shlomit Gilad; Adina Weinberger; Yael Kuperman; Alon Harmelin; Ilana Kolodkin-Gal; Hagit Shapiro; Zamir Halpern; Eran Segal; Eran Elinav;

  • 作者单位

    Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel;

    Department of Computer Science and Applied Mathematics, Weizmann Institute of Science, Rehovot 76100, Israel;

    Department of Computer Science and Applied Mathematics, Weizmann Institute of Science, Rehovot 76100, Israel;

    Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel;

    Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel;

    Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel;

    Day Care Unit and the Laboratory of Imaging and Brain Stimulation, Kfar Shaul hospital, Jerusalem Center for Mental Health, Jerusalem 91060, Israel;

    Internal Medicine Department Tel Aviv Sourasky Medical Center, Tel Aviv 64239, Israel,Research Center for Digestive Tract and Liver Diseases, Tel Aviv Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel,Digestive Center, Tel Aviv Sourasky Medical Center, Tel Aviv 64239, Israel;

    The Nancy and Stephen Grand Israel National Center for Personalized Medicine (INCPM), Weizmann Institute of Science, Rehovot 76100, Israel;

    Department of Computer Science and Applied Mathematics, Weizmann Institute of Science, Rehovot 76100, Israel;

    Department of Veterinary Resources, Weizmann Institute of Science, Rehovot 76100, Israel;

    Department of Veterinary Resources, Weizmann Institute of Science, Rehovot 76100, Israel;

    Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel;

    Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel;

    Research Center for Digestive Tract and Liver Diseases, Tel Aviv Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel,Digestive Center, Tel Aviv Sourasky Medical Center, Tel Aviv 64239, Israel;

    Department of Computer Science and Applied Mathematics, Weizmann Institute of Science, Rehovot 76100, Israel;

    Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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