Statin therapy is associated with lower prevalence of gut microbiota dysbiosis
Microbiome community typing analyses have recently identified the Bacteroides 2 (Bact2) enterotype, an intestinal microbiota configuration that is associated with systemic inflammation and has a high prevalence in loose stools in humans 1 , 2 . Bact2 is characterized by a high proportion of Bacteroi...
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| Published in: | Nature (London) Vol. 581; no. 7808; pp. 310 - 315 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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01-05-2020
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| Abstract | Microbiome community typing analyses have recently identified the
Bacteroides
2 (Bact2) enterotype, an intestinal microbiota configuration that is associated with systemic inflammation and has a high prevalence in loose stools in humans
1
,
2
. Bact2 is characterized by a high proportion of
Bacteroides
, a low proportion of
Faecalibacterium
and low microbial cell densities
1
,
2
, and its prevalence varies from 13% in a general population cohort to as high as 78% in patients with inflammatory bowel disease
2
. Reported changes in stool consistency
3
and inflammation status
4
during the progression towards obesity and metabolic comorbidities led us to propose that these developments might similarly correlate with an increased prevalence of the potentially dysbiotic Bact2 enterotype. Here, by exploring obesity-associated microbiota alterations in the quantitative faecal metagenomes of the cross-sectional MetaCardis Body Mass Index Spectrum cohort (
n
= 888), we identify statin therapy as a key covariate of microbiome diversification. By focusing on a subcohort of participants that are not medicated with statins, we find that the prevalence of Bact2 correlates with body mass index, increasing from 3.90% in lean or overweight participants to 17.73% in obese participants. Systemic inflammation levels in Bact2-enterotyped individuals are higher than predicted on the basis of their obesity status, indicative of Bact2 as a dysbiotic microbiome constellation. We also observe that obesity-associated microbiota dysbiosis is negatively associated with statin treatment, resulting in a lower Bact2 prevalence of 5.88% in statin-medicated obese participants. This finding is validated in both the accompanying MetaCardis cardiovascular disease dataset (
n
= 282) and the independent Flemish Gut Flora Project population cohort (
n =
2,345). The potential benefits of statins in this context will require further evaluation in a prospective clinical trial to ascertain whether the effect is reproducible in a randomized population and before considering their application as microbiota-modulating therapeutics.
A cross-sectional analysis of participants in the MetaCardis Body Mass Index Spectrum cohort finds that the higher prevalence of gut microbiota dysbiosis in individuals with obesity is not observed in those who take statin drugs. |
|---|---|
| AbstractList | Microbiome community typing analyses have recently identified the
Bacteroides
2 (Bact2) enterotype, an intestinal microbiota configuration that is associated with systemic inflammation and has a high prevalence in loose stools in humans
1
,
2
. Bact2 is characterized by a high proportion of
Bacteroides
, a low proportion of
Faecalibacterium
and low microbial cell densities
1
,
2
, and its prevalence varies from 13% in a general population cohort to as high as 78% in patients with inflammatory bowel disease
2
. Reported changes in stool consistency
3
and inflammation status
4
during the progression towards obesity and metabolic comorbidities led us to propose that these developments might similarly correlate with an increased prevalence of the potentially dysbiotic Bact2 enterotype. Here, by exploring obesity-associated microbiota alterations in the quantitative faecal metagenomes of the cross-sectional MetaCardis Body Mass Index Spectrum cohort (
n
= 888), we identify statin therapy as a key covariate of microbiome diversification. By focusing on a subcohort of participants that are not medicated with statins, we find that the prevalence of Bact2 correlates with body mass index, increasing from 3.90% in lean or overweight participants to 17.73% in obese participants. Systemic inflammation levels in Bact2-enterotyped individuals are higher than predicted on the basis of their obesity status, indicative of Bact2 as a dysbiotic microbiome constellation. We also observe that obesity-associated microbiota dysbiosis is negatively associated with statin treatment, resulting in a lower Bact2 prevalence of 5.88% in statin-medicated obese participants. This finding is validated in both the accompanying MetaCardis cardiovascular disease dataset (
n
= 282) and the independent Flemish Gut Flora Project population cohort (
n =
2,345). The potential benefits of statins in this context will require further evaluation in a prospective clinical trial to ascertain whether the effect is reproducible in a randomized population and before considering their application as microbiota-modulating therapeutics.
A cross-sectional analysis of participants in the MetaCardis Body Mass Index Spectrum cohort finds that the higher prevalence of gut microbiota dysbiosis in individuals with obesity is not observed in those who take statin drugs. Microbiome community typing analyses have recently identified the Bacteroides2 (Bact2) enterotype, an intestinal microbiota configuration that is associated with systemic inflammation and has a high prevalence in loose stools in humans.sup.1,2. Bact2 is characterized by a high proportion of Bacteroides, a low proportion of Faecalibacterium and low microbial cell densities.sup.1,2, and its prevalence varies from 13% in a general population cohort to as high as 78% in patients with inflammatory bowel disease.sup.2. Reported changes in stool consistency.sup.3 and inflammation status.sup.4 during the progression towards obesity and metabolic comorbidities led us to propose that these developments might similarly correlate with an increased prevalence of the potentially dysbiotic Bact2 enterotype. Here, by exploring obesity-associated microbiota alterations in the quantitative faecal metagenomes of the cross-sectional MetaCardis Body Mass Index Spectrum cohort (n = 888), we identify statin therapy as a key covariate of microbiome diversification. By focusing on a subcohort of participants that are not medicated with statins, we find that the prevalence of Bact2 correlates with body mass index, increasing from 3.90% in lean or overweight participants to 17.73% in obese participants. Systemic inflammation levels in Bact2-enterotyped individuals are higher than predicted on the basis of their obesity status, indicative of Bact2 as a dysbiotic microbiome constellation. We also observe that obesity-associated microbiota dysbiosis is negatively associated with statin treatment, resulting in a lower Bact2 prevalence of 5.88% in statin-medicated obese participants. This finding is validated in both the accompanying MetaCardis cardiovascular disease dataset (n = 282) and the independent Flemish Gut Flora Project population cohort (n = 2,345). The potential benefits of statins in this context will require further evaluation in a prospective clinical trial to ascertain whether the effect is reproducible in a randomized population and before considering their application as microbiota-modulating therapeutics. A cross-sectional analysis of participants in the MetaCardis Body Mass Index Spectrum cohort finds that the higher prevalence of gut microbiota dysbiosis in individuals with obesity is not observed in those who take statin drugs. Microbiome community typing analyses have recently identified the Bacteroides2 (Bact2) enterotype, an intestinal microbiota configuration that is associated with systemic inflammation and has a high prevalence in loose stools in humans1,2. Bact2 is characterized by a high proportion of Bacteroides, a low proportion of Faecalibacterium and low microbial cell densities1,2, and its prevalence varies from 13% in a general population cohort to as high as 78% in patients with inflammatory bowel disease2. Reported changes in stool consistency3 and inflammation status4 during the progression towards obesity and metabolic comorbidities led us to propose that these developments might similarly correlate with an increased prevalence of the potentially dysbiotic Bact2 enterotype. Here, by exploring obesity-associated microbiota alterations in the quantitative faecal metagenomes of the cross-sectional MetaCardis Body Mass Index Spectrum cohort (n=888), we identify statin therapy as a key covariate of microbiome diversification. By focusing on a subcohort of participants that are not medicated with statins, we find that the prevalence of Bact2 correlates with body mass index, increasing from 3.90% in lean or overweight participants to 17.73% in obese participants. Systemic inflammation levels in Bact2-enterotyped individuals are higher than predicted on the basis of their obesity status, indicative of Bact2 as a dysbiotic microbiome constellation. We also observe that obesity-associated microbiota dysbiosis is negatively associated with statin treatment, resulting in a lower Bact2 prevalence of 5.88% in statin-medicated obese participants. This finding is validated in both the accompanying MetaCardis cardiovascular disease dataset (n = 282) and the independent Flemish Gut Flora Project population cohort (n=2,345). The potential benefits of statins in this context will require further evaluation in a prospective clinical trial to ascertain whether the effect is reproducible in a randomized population and before considering their application as microbiota-modulating therapeutics. © 2020, The Author(s), under exclusive licence to Springer Nature Limited. Microbiome community typing analyses have recently identified the Bacteroides2 (Bact2) enterotype, an intestinal microbiota configuration that is associated with systemic inflammation and has a high prevalence in loose stools in humans1,2. Bact2 is characterized by a high proportion of Bacteroides, a low proportion of Faecalibacterium and low microbial cell densities1,2, and its prevalence varies from 13% in a general population cohort to as high as 78% in patients with inflammatory bowel disease2. Reported changes in stool consistency3 and inflammation status4 during the progression towards obesity and metabolic comorbidities led us to propose that these developments might similarly correlate with an increased prevalence of the potentially dysbiotic Bact2 enterotype. Here, by exploring obesity-associated microbiota alterations in the quantitative faecal metagenomes of the cross-sectional MetaCardis Body Mass Index Spectrum cohort (n = 888), we identify statin therapy as a key covariate of microbiome diversification. By focusing on a subcohort of participants that are not medicated with statins, we find that the prevalence of Bact2 correlates with body mass index, increasing from 3.90% in lean or overweight participants to 17.73% in obese participants. Systemic inflammation levels in Bact2-enterotyped individuals are higher than predicted on the basis of their obesity status, indicative of Bact2 as a dysbiotic microbiome constellation. We also observe that obesity-associated microbiota dysbiosis is negatively associated with statin treatment, resulting in a lower Bact2 prevalence of 5.88% in statin-medicated obese participants. This finding is validated in both the accompanying MetaCardis cardiovascular disease dataset (n = 282) and the independent Flemish Gut Flora Project population cohort (n = 2,345). The potential benefits of statins in this context will require further evaluation in a prospective clinical trial to ascertain whether the effect is reproducible in a randomized population and before considering their application as microbiota-modulating therapeutics. Microbiome community typing analyses have recently identified the Bacteroides2 (Bact2) enterotype, an intestinal microbiota configuration that is associated with systemic inflammation and has a high prevalence in loose stools in humans.sup.1,2. Bact2 is characterized by a high proportion of Bacteroides, a low proportion of Faecalibacterium and low microbial cell densities.sup.1,2, and its prevalence varies from 13% in a general population cohort to as high as 78% in patients with inflammatory bowel disease.sup.2. Reported changes in stool consistency.sup.3 and inflammation status.sup.4 during the progression towards obesity and metabolic comorbidities led us to propose that these developments might similarly correlate with an increased prevalence of the potentially dysbiotic Bact2 enterotype. Here, by exploring obesity-associated microbiota alterations in the quantitative faecal metagenomes of the cross-sectional MetaCardis Body Mass Index Spectrum cohort (n = 888), we identify statin therapy as a key covariate of microbiome diversification. By focusing on a subcohort of participants that are not medicated with statins, we find that the prevalence of Bact2 correlates with body mass index, increasing from 3.90% in lean or overweight participants to 17.73% in obese participants. Systemic inflammation levels in Bact2-enterotyped individuals are higher than predicted on the basis of their obesity status, indicative of Bact2 as a dysbiotic microbiome constellation. We also observe that obesity-associated microbiota dysbiosis is negatively associated with statin treatment, resulting in a lower Bact2 prevalence of 5.88% in statin-medicated obese participants. This finding is validated in both the accompanying MetaCardis cardiovascular disease dataset (n = 282) and the independent Flemish Gut Flora Project population cohort (n = 2,345). The potential benefits of statins in this context will require further evaluation in a prospective clinical trial to ascertain whether the effect is reproducible in a randomized population and before considering their application as microbiota-modulating therapeutics. Microbiome community typing analyses have recently identified the Bacteroides2 (Bact2) enterotype, an intestinal microbiota configuration that is associated with systemic inflammation and has a high prevalence in loose stools in humans1,2. Bact2 is characterized by a high proportion of Bacteroides, a low proportion of Faecalibacterium and low microbial cell densities1,2, and its prevalence varies from 13% in a general population cohort to as high as 78% in patients with inflammatory bowel disease2. Reported changes in stool consistency3 and inflammation status4 during the progression towards obesity and metabolic comorbidities led us to propose that these developments might similarly correlate with an increased prevalence of the potentially dysbiotic Bact2 enterotype. Here, by exploring obesity-associated microbiota alterations in the quantitative faecal metagenomes of the cross-sectional MetaCardis Body Mass Index Spectrum cohort (n = 888), we identify statin therapy as a key covariate of microbiome diversification. By focusing on a subcohort of participants that are not medicated with statins, we find that the prevalence of Bact2 correlates with body mass index, increasing from 3.90% in lean or overweight participants to 17.73% in obese participants. Systemic inflammation levels in Bact2-enterotyped individuals are higher than predicted on the basis of their obesity status, indicative of Bact2 as a dysbiotic microbiome constellation. We also observe that obesity-associated microbiota dysbiosis is negatively associated with statin treatment, resulting in a lower Bact2 prevalence of 5.88% in statin-medicated obese participants. This finding is validated in both the accompanying MetaCardis cardiovascular disease dataset (n = 282) and the independent Flemish Gut Flora Project population cohort (n = 2,345). The potential benefits of statins in this context will require further evaluation in a prospective clinical trial to ascertain whether the effect is reproducible in a randomized population and before considering their application as microbiota-modulating therapeutics. Microbiome community typing analyses have recently identified the Bacteroides2 (Bact2) enterotype, an intestinal microbiota configuration that is associated with systemic inflammation and has a high prevalence in loose stools in humans . Bact2 is characterized by a high proportion of Bacteroides, a low proportion of Faecalibacterium and low microbial cell densities , and its prevalence varies from 13% in a general population cohort to as high as 78% in patients with inflammatory bowel disease . Reported changes in stool consistency and inflammation status during the progression towards obesity and metabolic comorbidities led us to propose that these developments might similarly correlate with an increased prevalence of the potentially dysbiotic Bact2 enterotype. Here, by exploring obesity-associated microbiota alterations in the quantitative faecal metagenomes of the cross-sectional MetaCardis Body Mass Index Spectrum cohort (n = 888), we identify statin therapy as a key covariate of microbiome diversification. By focusing on a subcohort of participants that are not medicated with statins, we find that the prevalence of Bact2 correlates with body mass index, increasing from 3.90% in lean or overweight participants to 17.73% in obese participants. Systemic inflammation levels in Bact2-enterotyped individuals are higher than predicted on the basis of their obesity status, indicative of Bact2 as a dysbiotic microbiome constellation. We also observe that obesity-associated microbiota dysbiosis is negatively associated with statin treatment, resulting in a lower Bact2 prevalence of 5.88% in statin-medicated obese participants. This finding is validated in both the accompanying MetaCardis cardiovascular disease dataset (n = 282) and the independent Flemish Gut Flora Project population cohort (n = 2,345). The potential benefits of statins in this context will require further evaluation in a prospective clinical trial to ascertain whether the effect is reproducible in a randomized population and before considering their application as microbiota-modulating therapeutics. Microbiome community typing analyses have recently identified the Bacteroidesl (Bact2) enterotype, an intestinal microbiota configuration that is associated with systemic inflammation and has a high prevalence in loose stools in humans1,2. Bact2 is characterized by a high proportion of Bacteroides, a low proportion of Faecalibacterium and low microbial cell densities1,2, and its prevalence varies from 13% in a general population cohort to as high as 78% in patients with inflammatory bowel disease2. Reported changes in stool consistency3 and inflammation status4 during the progression towards obesity and metabolic comorbidities led us to propose that these developments might similarly correlate with an increased prevalence of the potentially dysbiotic Bact2 enterotype. Here, by exploring obesity-associated microbiota alterations in the quantitative faecal metagenomes of the cross-sectional MetaCardis Body Mass Index Spectrum cohort (n = 888), we identify statin therapy as a key covariate of microbiome diversification. By focusing on a subcohort of participants that are not medicated with statins, we find that the prevalence of Bact2 correlates with body mass index, increasing from 3.90% in lean or overweight participants to 17.73% in obese participants. Systemic inflammation levels in Bact2-enterotyped individuals are higher than predicted on the basis of their obesity status, indicative of Bact2 as a dysbiotic microbiome constellation. We also observe that obesity-associated microbiota dysbiosis is negatively associated with statin treatment, resulting in a lower Bact2 prevalence of 5.88% in statin-medicated obese participants. This finding is validated in both the accompanying MetaCardis cardiovascular disease dataset (n = 282) and the independent Flemish Gut Flora Project population cohort (n = 2,345). The potential benefits of statins in this context will require further evaluation in a prospective clinical trial to ascertain whether the effect is reproducible in a randomized population and before considering their application as microbiota-modulating therapeutics. |
| Audience | Academic |
| Author | Pons, Nicolas Andreelli, Fabrizio Coelho, Luis Pedro Gøtze, Jens P. Tremaroli, Valentina Bork, Peer Clément, Karine Roume, Hugo Bastard, Jean-Phillippe Oppert, Jean-Michel Pedersen, Helle K. Rouault, Christine Vieira-Silva, Sara Chakaroun, Rima Forslund, Sofia K. Valles-Colomer, Mireia Assmann, Karen Aron-Wisnewsky, Judith Ehrlich, Stanislav Dusko Nielsen, Trine Bäckhed, Fredrik Belda, Eugeni Pedersen, Oluf Prifti, Edi Le Chatelier, Emmanuelle Holst, Jens J. Nielsen, Jens Letunic, Ivica Nguyen, Thi Thuy Duyen Lewinter, Christian Hulot, Jean-Sébastien Zucker, Jean-Daniel Køber, Lars Proost, Sebastian Quinquis, Benoit Falony, Gwen Galan, Pilar Touch, Sothea Hansen, Torben Vestergaard, Henrik Hansen, Tue H. Galleron, Nathalie Salem, Joe-Elie Stumvoll, Michael Dumas, Marc-Emmanuel Søndertoft, Nadja B. Raes, Jeroen |
| Author_xml | – sequence: 1 givenname: Sara orcidid: 0000-0002-4616-7602 surname: Vieira-Silva fullname: Vieira-Silva, Sara organization: Laboratory of Molecular Bacteriology, Department of Microbiology and Immunology, Rega Institute, KU Leuven, Center for Microbiology, VIB – sequence: 2 givenname: Gwen surname: Falony fullname: Falony, Gwen organization: Laboratory of Molecular Bacteriology, Department of Microbiology and Immunology, Rega Institute, KU Leuven, Center for Microbiology, VIB – sequence: 3 givenname: Eugeni surname: Belda fullname: Belda, Eugeni organization: Nutrition and Obesities: Systemic Approaches Research Unit (NutriOmics), INSERM, Sorbonne Université, Institute of Cardiometabolism and Nutrition, Integromics Unit – sequence: 4 givenname: Trine orcidid: 0000-0002-2066-7895 surname: Nielsen fullname: Nielsen, Trine organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen – sequence: 5 givenname: Judith surname: Aron-Wisnewsky fullname: Aron-Wisnewsky, Judith organization: Nutrition and Obesities: Systemic Approaches Research Unit (NutriOmics), INSERM, Sorbonne Université, Nutrition Department, Pitie-Salpêtrière Hospital, Assistance Publique Hôpitaux de Paris – sequence: 6 givenname: Rima surname: Chakaroun fullname: Chakaroun, Rima organization: Medical Department III – Endocrinology, Nephrology, Rheumatology, University of Leipzig Medical Center – sequence: 7 givenname: Sofia K. surname: Forslund fullname: Forslund, Sofia K. organization: Experimental and Clinical Research Center, Charité-Universitätsmedizin and Max-Delbrück Center, Structural and Computational Biology, European Molecular Biology Laboratory, Max Delbruck Center for Molecular Medicine in the Helmholtz Association (MDC), DZHK (German Centre for Cardiovascular Research), Partner Site Berlin – sequence: 8 givenname: Karen surname: Assmann fullname: Assmann, Karen organization: Nutrition and Obesities: Systemic Approaches Research Unit (NutriOmics), INSERM, Sorbonne Université – sequence: 9 givenname: Mireia surname: Valles-Colomer fullname: Valles-Colomer, Mireia organization: Laboratory of Molecular Bacteriology, Department of Microbiology and Immunology, Rega Institute, KU Leuven, Center for Microbiology, VIB – sequence: 10 givenname: Thi Thuy Duyen surname: Nguyen fullname: Nguyen, Thi Thuy Duyen organization: Laboratory of Molecular Bacteriology, Department of Microbiology and Immunology, Rega Institute, KU Leuven, Center for Microbiology, VIB – sequence: 11 givenname: Sebastian orcidid: 0000-0002-6792-9442 surname: Proost fullname: Proost, Sebastian organization: Laboratory of Molecular Bacteriology, Department of Microbiology and Immunology, Rega Institute, KU Leuven, Center for Microbiology, VIB – sequence: 12 givenname: Edi orcidid: 0000-0001-8861-1305 surname: Prifti fullname: Prifti, Edi organization: Nutrition and Obesities: Systemic Approaches Research Unit (NutriOmics), INSERM, Sorbonne Université, Institute of Cardiometabolism and Nutrition, Integromics Unit, Unité de Modélisation Mathématique et Informatique des Systèmes Complexes, UMMISCO, Sorbonne Université, IRD – sequence: 13 givenname: Valentina surname: Tremaroli fullname: Tremaroli, Valentina organization: Wallenberg Laboratory, Department of Molecular and Clinical Medicine and Sahlgrenska Academy, University of Gothenburg – sequence: 14 givenname: Nicolas surname: Pons fullname: Pons, Nicolas organization: Université Paris-Saclay, INRAE, Metagenopolis – sequence: 15 givenname: Emmanuelle surname: Le Chatelier fullname: Le Chatelier, Emmanuelle organization: Université Paris-Saclay, INRAE, Metagenopolis – sequence: 16 givenname: Fabrizio surname: Andreelli fullname: Andreelli, Fabrizio organization: Nutrition and Obesities: Systemic Approaches Research Unit (NutriOmics), INSERM, Sorbonne Université, Diabetes Department, Pitie-Salpêtrière Hospital, Assistance Publique Hôpitaux de Paris – sequence: 17 givenname: Jean-Phillippe surname: Bastard fullname: Bastard, Jean-Phillippe organization: UF Biomarqueurs Inflammatoires et Métaboliques, Biochemistry and Hormonology Department, Tenon Hospital, Assistance Publique Hôpitaux de Paris, Centre de Recherche Saint-Antoine, Sorbonne Université-INSERM UMR-S 938, IHU ICAN – sequence: 18 givenname: Luis Pedro orcidid: 0000-0002-9280-7885 surname: Coelho fullname: Coelho, Luis Pedro organization: Structural and Computational Biology, European Molecular Biology Laboratory, Institute of Science and Technology for Brain-Inspired Intelligence, Fudan University – sequence: 19 givenname: Nathalie surname: Galleron fullname: Galleron, Nathalie organization: Université Paris-Saclay, INRAE, Metagenopolis – sequence: 20 givenname: Tue H. surname: Hansen fullname: Hansen, Tue H. organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen – sequence: 21 givenname: Jean-Sébastien surname: Hulot fullname: Hulot, Jean-Sébastien organization: NICO Cardio-oncology Program, CIC-1421, Department of Pharmacology, Pitié-Salpêtrière Hospital, Assistance Publique Hôpitaux de Paris, INSERM, Sorbonne Université, Université de Paris, PARCC, INSERM, CIC1418 and DMU CARTE, Assistance Publique–Hôpitaux de Paris, Hôpital Européen Georges-Pompidou – sequence: 22 givenname: Christian surname: Lewinter fullname: Lewinter, Christian organization: Department of Cardiology, Rigshospitalet, University of Copenhagen – sequence: 23 givenname: Helle K. surname: Pedersen fullname: Pedersen, Helle K. organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen – sequence: 24 givenname: Benoit surname: Quinquis fullname: Quinquis, Benoit organization: Université Paris-Saclay, INRAE, Metagenopolis – sequence: 25 givenname: Christine surname: Rouault fullname: Rouault, Christine organization: Nutrition and Obesities: Systemic Approaches Research Unit (NutriOmics), INSERM, Sorbonne Université – sequence: 26 givenname: Hugo surname: Roume fullname: Roume, Hugo organization: Université Paris-Saclay, INRAE, Metagenopolis – sequence: 27 givenname: Joe-Elie surname: Salem fullname: Salem, Joe-Elie organization: NICO Cardio-oncology Program, CIC-1421, Department of Pharmacology, Pitié-Salpêtrière Hospital, Assistance Publique Hôpitaux de Paris, INSERM, Sorbonne Université – sequence: 28 givenname: Nadja B. orcidid: 0000-0001-6350-8117 surname: Søndertoft fullname: Søndertoft, Nadja B. organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen – sequence: 29 givenname: Sothea surname: Touch fullname: Touch, Sothea organization: Nutrition and Obesities: Systemic Approaches Research Unit (NutriOmics), INSERM, Sorbonne Université – sequence: 31 givenname: Marc-Emmanuel orcidid: 0000-0001-9523-7024 surname: Dumas fullname: Dumas, Marc-Emmanuel organization: Computational and Systems Medicine, Department of Metabolism, Digestion and Reproduction, Faculty of Medicine, Imperial College London, Genomic and Environmental Medicine, National Heart & Lung Institute, Faculty of Medicine, Imperial College London – sequence: 32 givenname: Stanislav Dusko orcidid: 0000-0002-7563-4046 surname: Ehrlich fullname: Ehrlich, Stanislav Dusko organization: Université Paris-Saclay, INRAE, Metagenopolis – sequence: 33 givenname: Pilar orcidid: 0000-0003-1706-3107 surname: Galan fullname: Galan, Pilar organization: Sorbonne Paris Cité Epidemiology and Statistics Research Centre (CRESS), U1153 INSERM, U1125, INRA, CNAM, University of Paris, Nutritional Epidemiology Research Team (EREN) – sequence: 34 givenname: Jens P. surname: Gøtze fullname: Gøtze, Jens P. organization: Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen – sequence: 35 givenname: Torben orcidid: 0000-0001-8748-3831 surname: Hansen fullname: Hansen, Torben organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen – sequence: 36 givenname: Jens J. orcidid: 0000-0001-6853-3805 surname: Holst fullname: Holst, Jens J. organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen – sequence: 37 givenname: Lars surname: Køber fullname: Køber, Lars organization: Department of Cardiology, Rigshospitalet, University of Copenhagen – sequence: 38 givenname: Ivica orcidid: 0000-0003-3560-4288 surname: Letunic fullname: Letunic, Ivica organization: Biobyte Solutions – sequence: 39 givenname: Jens orcidid: 0000-0002-9955-6003 surname: Nielsen fullname: Nielsen, Jens organization: Department of Biology and Biological Engineering, Chalmers University of Technology – sequence: 40 givenname: Jean-Michel surname: Oppert fullname: Oppert, Jean-Michel organization: Nutrition Department, Pitie-Salpêtrière Hospital, Assistance Publique Hôpitaux de Paris – sequence: 41 givenname: Michael surname: Stumvoll fullname: Stumvoll, Michael organization: Medical Department III – Endocrinology, Nephrology, Rheumatology, University of Leipzig Medical Center, Helmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG) of the Helmholtz Zentrum München at the University of Leipzig – sequence: 42 givenname: Henrik orcidid: 0000-0003-3090-269X surname: Vestergaard fullname: Vestergaard, Henrik organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen – sequence: 43 givenname: Jean-Daniel surname: Zucker fullname: Zucker, Jean-Daniel organization: Nutrition and Obesities: Systemic Approaches Research Unit (NutriOmics), INSERM, Sorbonne Université, Institute of Cardiometabolism and Nutrition, Integromics Unit, Unité de Modélisation Mathématique et Informatique des Systèmes Complexes, UMMISCO, Sorbonne Université, IRD – sequence: 44 givenname: Peer orcidid: 0000-0002-2627-833X surname: Bork fullname: Bork, Peer organization: Structural and Computational Biology, European Molecular Biology Laboratory, Molecular Medicine Partnership Unit, University of Heidelberg and European Molecular Biology Laboratory, Department of Bioinformatics, Biocenter, University of Würzburg – sequence: 45 givenname: Oluf orcidid: 0000-0002-3321-3972 surname: Pedersen fullname: Pedersen, Oluf organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen – sequence: 46 givenname: Fredrik surname: Bäckhed fullname: Bäckhed, Fredrik organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Wallenberg Laboratory, Department of Molecular and Clinical Medicine and Sahlgrenska Academy, University of Gothenburg – sequence: 47 givenname: Karine orcidid: 0000-0002-2489-3355 surname: Clément fullname: Clément, Karine email: karine.clement@inserm.fr organization: Nutrition and Obesities: Systemic Approaches Research Unit (NutriOmics), INSERM, Sorbonne Université, Nutrition Department, Pitie-Salpêtrière Hospital, Assistance Publique Hôpitaux de Paris – sequence: 48 givenname: Jeroen orcidid: 0000-0002-1337-041X surname: Raes fullname: Raes, Jeroen email: jeroen.raes@kuleuven.be organization: Laboratory of Molecular Bacteriology, Department of Microbiology and Immunology, Rega Institute, KU Leuven, Center for Microbiology, VIB |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32433607$$D View this record in MEDLINE/PubMed https://hal.inrae.fr/hal-02964351$$DView record in HAL https://gup.ub.gu.se/publication/296905$$DView record from Swedish Publication Index https://research.chalmers.se/publication/517357$$DView record from Swedish Publication Index |
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| ContentType | Journal Article |
| Contributor | Hartmann, Bolette Kuhn, Michael Poitou-Bernert, Christine Galijatovic, Ehm Astrid Andersson Kerneis, Mathieu Helft, Gerard Massey, Robin Le Pavin, Laetitia Pasero Camus, Mickael Djebbar, Morad Ciangura, Cecile Fromentin, Sebastien Batisse, Jean-Paul Isnard, Richard Cassuto, Dominique Khemis, Jean Boubrit, Rachid Moitinho-Silva, Lucas Svendstrup, Mathilde Moutel, Sandrine Debedat, Jean Schmidt, Sebastian Kammer, Judith Alves, Renato Amouyal, Chloe Berland, Magalie Bittar, Randa Jaqueminet, Sophie Justesen, Johanne Medina-Stamminger, Jonathan Verger, Eric Fellahi, Soraya Maziers, Nicolas Vatier, Camille Lucas-Martini, Lea Doré, Angélique Krarup, Nikolaj Blottière, Hervé Vanduyvenboden, Thierry Engelbrechtsen, Line Graine, Marianne Barthelemy, Olivier Hornbak, Malene Bosquet, Frederic Hartemann, Agnes Bourron, Olivier Lejard, Véronique Montalescot, Gilles Walther, Stefanie Levenez, Florence Pousset, Francoise Pouzoulet, Laurence Jørgensen, Niklas Rye Julienne, Hanna Swartz, Timothy Hercberg, Serge Dao, Maria-Carlota Collet, Jean-Philippe Lampuré |
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| Copyright | The Author(s), under exclusive licence to Springer Nature Limited 2020 COPYRIGHT 2020 Nature Publishing Group Copyright Nature Publishing Group May 21, 2020 Distributed under a Creative Commons Attribution 4.0 International License |
| Copyright_xml | – notice: The Author(s), under exclusive licence to Springer Nature Limited 2020 – notice: COPYRIGHT 2020 Nature Publishing Group – notice: Copyright Nature Publishing Group May 21, 2020 – notice: Distributed under a Creative Commons Attribution 4.0 International License |
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| References | Quévrain (CR15) 2016; 65 Grant (CR54) 2014; 348 Ridker (CR23) 2009; 373 Gardiner (CR20) 2015; 53 Forslund (CR27) 2015; 528 Le Chatelier (CR8) 2013; 500 CR36 Falony, Vieira-Silva, Raes (CR41) 2015; 69 Grip, Janciauskiene, Bredberg (CR29) 2008; 155 Turnbaugh (CR5) 2006; 444 Louis (CR16) 2004; 186 Khan (CR25) 2018; 8 Litvak, Byndloss, Bäumler (CR17) 2018; 362 Touch (CR32) 2018; 32 Walters, Xu, Knight (CR7) 2014; 588 Muscogiuri (CR24) 2014; 39 Probert, Emmett, Heaton (CR3) 1995; 88 Depommier (CR13) 2019; 25 Karlsson (CR9) 2012; 3 Ford (CR4) 1999; 22 Cotillard (CR35) 2013; 500 Valles-Colomer (CR31) 2019; 4 Darzi, Falony, Vieira-Silva, Raes (CR42) 2016; 10 Zeiser (CR28) 2018; 154 Yun (CR14) 2017; 17 CR49 CR48 CR47 CR45 Vieira-Silva (CR11) 2016; 1 CR43 Duvallet, Gibbons, Gurry, Irizarry, Alm (CR53) 2017; 8 Kultima (CR37) 2016; 32 Ungaro (CR30) 2016; 111 Kriss, Hazleton, Nusbacher, Martin, Lozupone (CR18) 2018; 44 Sze, Schloss (CR6) 2016; 7 Wexler (CR22) 2007; 20 Vandeputte (CR1) 2017; 551 CR51 CR50 Mazmanian, Liu, Tzianabos, Kasper (CR21) 2005; 122 Maier (CR26) 2018; 555 Holmes, Harris, Quince (CR52) 2012; 7 Vieira-Silva (CR2) 2019; 4 Prest, Hammes, Kötzsch, van Loosdrecht, Vrouwenvelder (CR39) 2013; 47 Ding, Schloss (CR19) 2014; 509 McMurdie, Holmes (CR44) 2013; 8 Criscuolo, Brisse (CR33) 2013; 102 Falony (CR10) 2016; 352 Nielsen (CR38) 2014; 32 Li (CR34) 2014; 32 Kultima (CR40) 2012; 7 Alberti, Zimmet, Shaw (CR12) 2006; 23 Hothorn, Hornik, van de Wiel, Zeileis (CR46) 2006; 60 32439977 - Nat Rev Cardiol. 2020 Jul;17(7):385 32376936 - Nature. 2020 May;581(7808):263-264 32827500 - Kidney Int. 2021 Mar;99(3):531-533 PM Ridker (2269_CR23) 2009; 373 2269_CR51 2269_CR50 I Holmes (2269_CR52) 2012; 7 HM Wexler (2269_CR22) 2007; 20 EI Prest (2269_CR39) 2013; 47 CS Probert (2269_CR3) 1995; 88 PJ Turnbaugh (2269_CR5) 2006; 444 KGMM Alberti (2269_CR12) 2006; 23 A Cotillard (2269_CR35) 2013; 500 C Depommier (2269_CR13) 2019; 25 T Ding (2269_CR19) 2014; 509 C Duvallet (2269_CR53) 2017; 8 D Vandeputte (2269_CR1) 2017; 551 MA Sze (2269_CR6) 2016; 7 E Le Chatelier (2269_CR8) 2013; 500 WA Walters (2269_CR7) 2014; 588 RL Grant (2269_CR54) 2014; 348 Y Litvak (2269_CR17) 2018; 362 PJ McMurdie (2269_CR44) 2013; 8 M Kriss (2269_CR18) 2018; 44 ES Ford (2269_CR4) 1999; 22 S Vieira-Silva (2269_CR11) 2016; 1 G Falony (2269_CR41) 2015; 69 FH Karlsson (2269_CR9) 2012; 3 T Hothorn (2269_CR46) 2006; 60 J Li (2269_CR34) 2014; 32 TJ Khan (2269_CR25) 2018; 8 JR Kultima (2269_CR37) 2016; 32 2269_CR36 G Muscogiuri (2269_CR24) 2014; 39 R Zeiser (2269_CR28) 2018; 154 A Criscuolo (2269_CR33) 2013; 102 HB Nielsen (2269_CR38) 2014; 32 L Maier (2269_CR26) 2018; 555 JR Kultima (2269_CR40) 2012; 7 Y Darzi (2269_CR42) 2016; 10 S Vieira-Silva (2269_CR2) 2019; 4 2269_CR48 P Louis (2269_CR16) 2004; 186 2269_CR47 E Quévrain (2269_CR15) 2016; 65 2269_CR45 G Falony (2269_CR10) 2016; 352 2269_CR43 R Ungaro (2269_CR30) 2016; 111 O Grip (2269_CR29) 2008; 155 S Touch (2269_CR32) 2018; 32 2269_CR49 BJ Gardiner (2269_CR20) 2015; 53 M Valles-Colomer (2269_CR31) 2019; 4 Y Yun (2269_CR14) 2017; 17 K Forslund (2269_CR27) 2015; 528 SK Mazmanian (2269_CR21) 2005; 122 |
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| Snippet | Microbiome community typing analyses have recently identified the
Bacteroides
2 (Bact2) enterotype, an intestinal microbiota configuration that is associated... Microbiome community typing analyses have recently identified the Bacteroides2 (Bact2) enterotype, an intestinal microbiota configuration that is associated... Microbiome community typing analyses have recently identified the Bacteroidesl (Bact2) enterotype, an intestinal microbiota configuration that is associated... |
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| Title | Statin therapy is associated with lower prevalence of gut microbiota dysbiosis |
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