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Disentangling type 2 diabetes and metformin treatment signatures in the human gut microbiota

机译：剖析人类肠道菌群中的2型糖尿病和二甲双胍治疗特征

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摘要

In recent years, several associations between common chronic human disorders and altered gut microbiome composition and function have been reported(1,2). In most of these reports, treatment regimens were not controlled for and conclusions could thus be confounded by the effects of various drugs on the microbiota, which may obscure microbial causes, protective factors or diagnostically relevant signals. Our study addresses disease and drug signatures in the human gut microbiome of type 2 diabetes mellitus (T2D). Two previous quantitative gut metagenomics studies of T2D patients that were unstratified for treatment yielded divergent conclusions regarding its associated gut microbial dysbiosis(3,4). Here we show, using 784 available human gut metagenomes, how antidiabetic medication confounds these results, and analyse in detail the effects of the most widely used antidiabetic drug metformin. We provide support for microbial mediation of the therapeutic effects of metformin through short-chain fatty acid production, as well as for potential microbiota-mediated mechanisms behind known intestinal adverse effects in the form of a relative increase in abundance of Escherichia species. Controlling for metformin treatment, we report a unified signature of gut microbiome shifts in T2D with a depletion of butyrate-producing taxa(3,4). These in turn cause functional microbiome shifts, in part alleviated by metformin-induced changes. Overall, the present study emphasizes the need to disentangle gut microbiota signatures of specific human diseases from those of medication.
机译：近年来，已经报道了常见的慢性人类疾病与肠道微生物组组成和功能改变之间的几种关联（1,2）。在大多数这些报告中，治疗方案没有得到控制，因此各种药物对微生物群的作用可能会混淆结论，这可能会掩盖微生物原因，保护性因素或诊断相关信号。我们的研究针对2型糖尿病（T2D）人体肠道微生物组中的疾病和药物特征。之前有两项针对T2D患者的未量化治疗的肠道肠道宏基因组学研究就其相关的肠道微生物营养不良得出了不同的结论（3,4）。在这里，我们展示了使用784种可用的人类肠道元基因组，抗糖尿病药物如何混淆这些结果，并详细分析了最广泛使用的抗糖尿病药物二甲双胍的作用。我们为通过短链脂肪酸产生的二甲双胍的治疗效果的微生物介导提供了支持，并为大肠杆菌的丰富度相对增加形式的已知肠道不利作用背后的潜在微生物介导的机制提供了支持。控制二甲双胍的治疗，我们报告了在T2D中肠道微生物组转移的统一特征，其中包括产生丁酸盐的类群的耗竭（3,4）。这些反过来引起功能性微生物组转移，部分地由二甲双胍诱导的变化减轻。总体而言，本研究强调需要从药物中分离出特定人类疾病的肠道微生物群特征。

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  • 来源
    《Nature》 |2015年第7581期|262-266|共5页
  • 作者

    Forslund Kristoffer; Hildebrand Falk; Nielsen Trine; Falony Gwen; Le Chatelier Emmanuelle; Sunagawa Shinichi; Prifti Edi; Vieira-Silva Sara; Gudmundsdottir Valborg; Pedersen Helle Krogh; Arumugam Manimozhiyan; Kristiansen Karsten; Voigt Anita Yvonne; Vestergaard Henrik; Hercog Rajna; Costea Paul Igor; Kultima Jens Roat; Li Junhua; Jorgensen Torben; Levenez Florence; Dore Joel; Nielsen H. Bjorn; Brunak Soren; Raes Jeroen; Hansen Torben; Wang Jun; Ehrlich S. Dusko; Bork Peer; Pedersen Oluf;

  • 作者单位

    European Mol Biol Lab, Struct & Computat Biol Unit, D-69117 Heidelberg, Germany;

    European Mol Biol Lab, Struct & Computat Biol Unit, D-69117 Heidelberg, Germany|Katholieke Univ Leuven, VIB Ctr Biol Dis, B-3000 Leuven, Belgium|Vrije Univ Brussel, Dept Biosci Engn, B-1040 Brussels, Belgium;

    Univ Copenhagen, Fac Hlth & Med Sci, Novo Nordisk Fdn, Ctr Basic Metab Res, DK-2200 Copenhagen, Denmark;

    Katholieke Univ Leuven, VIB Ctr Biol Dis, B-3000 Leuven, Belgium|Katholieke Univ Leuven, Rega Inst Med Res, Dept Microbiol & Immunol, Lab Mol Bacteriol, B-3000 Leuven, Belgium;

    INRA, MICALIS, F-78352 Jouy En Josas, France|INRA, Metagenopolis, F-78352 Jouy En Josas, France;

    European Mol Biol Lab, Struct & Computat Biol Unit, D-69117 Heidelberg, Germany;

    INRA, MICALIS, F-78352 Jouy En Josas, France|INRA, Metagenopolis, F-78352 Jouy En Josas, France|Inst Cardiometab & Nutr, F-75013 Paris, France;

    Katholieke Univ Leuven, VIB Ctr Biol Dis, B-3000 Leuven, Belgium|Katholieke Univ Leuven, Rega Inst Med Res, Dept Microbiol & Immunol, Lab Mol Bacteriol, B-3000 Leuven, Belgium;

    Tech Univ Denmark, Ctr Biol Sequence Anal, Dept Syst Biol, DK-2800 Lyngby, Denmark;

    Tech Univ Denmark, Ctr Biol Sequence Anal, Dept Syst Biol, DK-2800 Lyngby, Denmark;

    Univ Copenhagen, Fac Hlth & Med Sci, Novo Nordisk Fdn, Ctr Basic Metab Res, DK-2200 Copenhagen, Denmark;

    Univ Copenhagen, Dept Biol, DK-2100 Copenhagen, Denmark;

    European Mol Biol Lab, Struct & Computat Biol Unit, D-69117 Heidelberg, Germany|Univ Heidelberg Hosp, Inst Pathol, Dept Appl Tumor Biol, D-69120 Heidelberg, Germany|Heidelberg Univ, Mol Med Partnership Unit, D-69120 Heidelberg, Germany|European Mol Biol Lab, D-69120 Heidelberg, Germany;

    Univ Copenhagen, Fac Hlth & Med Sci, Novo Nordisk Fdn, Ctr Basic Metab Res, DK-2200 Copenhagen, Denmark;

    European Mol Biol Lab, Struct & Computat Biol Unit, D-69117 Heidelberg, Germany;

    European Mol Biol Lab, Struct & Computat Biol Unit, D-69117 Heidelberg, Germany;

    European Mol Biol Lab, Struct & Computat Biol Unit, D-69117 Heidelberg, Germany;

    Bejing Genom Inst BGI Shenzhen, Shenzhen 518083, Peoples R China;

    Capital Reg Denmark, Res Ctr Prevent & Hlth, DK-2600 Glostrup, Denmark|Univ Copenhagen, Fac Hlth & Med Sci, Dept Publ Hlth, DK-2600 Copenhagen, Denmark|Aalborg Univ, Fac Med, DK-9100 Aalborg, Denmark;

    INRA, MICALIS, F-78352 Jouy En Josas, France|INRA, Metagenopolis, F-78352 Jouy En Josas, France;

    INRA, MICALIS, F-78352 Jouy En Josas, France|INRA, Metagenopolis, F-78352 Jouy En Josas, France;

    Tech Univ Denmark, Ctr Biol Sequence Anal, Dept Syst Biol, DK-2800 Lyngby, Denmark;

    Tech Univ Denmark, Ctr Biol Sequence Anal, Dept Syst Biol, DK-2800 Lyngby, Denmark|Univ Copenhagen, Fac Hlth & Med Sci, Novo Nordisk Fdn, Ctr Prot Res,Dis Syst Biol, DK-2200 Copenhagen, Denmark;

    Katholieke Univ Leuven, VIB Ctr Biol Dis, B-3000 Leuven, Belgium|Vrije Univ Brussel, Dept Biosci Engn, B-1040 Brussels, Belgium|Katholieke Univ Leuven, Rega Inst Med Res, Dept Microbiol & Immunol, Lab Mol Bacteriol, B-3000 Leuven, Belgium;

    Univ Copenhagen, Fac Hlth & Med Sci, Novo Nordisk Fdn, Ctr Basic Metab Res, DK-2200 Copenhagen, Denmark|Univ Southern Denmark, Fac Hlth Sci, DK-5000 Odense, Denmark;

    Univ Copenhagen, Dept Biol, DK-2100 Copenhagen, Denmark|Bejing Genom Inst BGI Shenzhen, Shenzhen 518083, Peoples R China|King Abdulaziz Univ, Princess Al Jawhara Albrahim Ctr Excellence Res H, Jeddah 80205, Saudi Arabia|Macau Univ Sci & Technol, Taipa, Macau, Peoples R China|Univ Hong Kong, Dept Med, Hong Kong, Hong Kong, Peoples R China|Univ Hong Kong, State Key Lab Pharmaceut Biotechnol, Hong Kong, Hong Kong, Peoples R China;

    INRA, MICALIS, F-78352 Jouy En Josas, France|INRA, Metagenopolis, F-78352 Jouy En Josas, France|Kings Coll London, Guys Hosp, Dent Inst Cent Off, Ctr Host Microbiome Interact, London SE1 9RT, England;

    European Mol Biol Lab, Struct & Computat Biol Unit, D-69117 Heidelberg, Germany|Heidelberg Univ, Mol Med Partnership Unit, D-69120 Heidelberg, Germany|European Mol Biol Lab, D-69120 Heidelberg, Germany|Max Delbruck Ctr Mol Med, D-13125 Berlin, Germany|Univ Wurzburg, Dept Bioinformat, D-97074 Wurzburg, Germany;

    Univ Copenhagen, Fac Hlth & Med Sci, Novo Nordisk Fdn, Ctr Basic Metab Res, DK-2200 Copenhagen, Denmark;

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