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High fat diet drives obesity regardless the composition of gut microbiota in mice

The gut microbiota is involved in many aspects of host physiology but its role in body weight and glucose metabolism remains unclear. Here we studied the compositional changes of gut microbiota in diet-induced obesity mice that were conventionally raised or received microbiota transplantation. In co...

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Autores principales: Rabot, Sylvie, Membrez, Mathieu, Blancher, Florence, Berger, Bernard, Moine, Déborah, Krause, Lutz, Bibiloni, Rodrigo, Bruneau, Aurélia, Gérard, Philippe, Siddharth, Jay, Lauber, Christian L., Chou, Chieh Jason
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5006052/
https://www.ncbi.nlm.nih.gov/pubmed/27577172
http://dx.doi.org/10.1038/srep32484
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author Rabot, Sylvie
Membrez, Mathieu
Blancher, Florence
Berger, Bernard
Moine, Déborah
Krause, Lutz
Bibiloni, Rodrigo
Bruneau, Aurélia
Gérard, Philippe
Siddharth, Jay
Lauber, Christian L.
Chou, Chieh Jason
author_facet Rabot, Sylvie
Membrez, Mathieu
Blancher, Florence
Berger, Bernard
Moine, Déborah
Krause, Lutz
Bibiloni, Rodrigo
Bruneau, Aurélia
Gérard, Philippe
Siddharth, Jay
Lauber, Christian L.
Chou, Chieh Jason
author_sort Rabot, Sylvie
collection PubMed
description The gut microbiota is involved in many aspects of host physiology but its role in body weight and glucose metabolism remains unclear. Here we studied the compositional changes of gut microbiota in diet-induced obesity mice that were conventionally raised or received microbiota transplantation. In conventional mice, the diversity of the faecal microbiota was weakly associated with 1(st) week weight gain but transferring the microbiota of mice with contrasting weight gain to germfree mice did not change obesity development or feed efficiency of recipients regardless whether the microbiota was taken before or after 10 weeks high fat (HF) feeding. Interestingly, HF-induced glucose intolerance was influenced by microbiota inoculation and improved glucose tolerance was associated with a low Firmicutes to Bacteroidetes ratio. Transplantation of Bacteroidetes rich microbiota compared to a control microbiota ameliorated glucose intolerance caused by HF feeding. Altogether, our results demonstrate that gut microbiota is involved in the regulation of glucose metabolism and the abundance of Bacteroidetes significantly modulates HF-induced glucose intolerance but has limited impact on obesity in mice. Our results suggest that gut microbiota is a part of complex aetiology of insulin resistance syndrome, individual microbiota composition may cause phenotypic variation associated with HF feeding in mice.
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spelling pubmed-50060522016-09-07 High fat diet drives obesity regardless the composition of gut microbiota in mice Rabot, Sylvie Membrez, Mathieu Blancher, Florence Berger, Bernard Moine, Déborah Krause, Lutz Bibiloni, Rodrigo Bruneau, Aurélia Gérard, Philippe Siddharth, Jay Lauber, Christian L. Chou, Chieh Jason Sci Rep Article The gut microbiota is involved in many aspects of host physiology but its role in body weight and glucose metabolism remains unclear. Here we studied the compositional changes of gut microbiota in diet-induced obesity mice that were conventionally raised or received microbiota transplantation. In conventional mice, the diversity of the faecal microbiota was weakly associated with 1(st) week weight gain but transferring the microbiota of mice with contrasting weight gain to germfree mice did not change obesity development or feed efficiency of recipients regardless whether the microbiota was taken before or after 10 weeks high fat (HF) feeding. Interestingly, HF-induced glucose intolerance was influenced by microbiota inoculation and improved glucose tolerance was associated with a low Firmicutes to Bacteroidetes ratio. Transplantation of Bacteroidetes rich microbiota compared to a control microbiota ameliorated glucose intolerance caused by HF feeding. Altogether, our results demonstrate that gut microbiota is involved in the regulation of glucose metabolism and the abundance of Bacteroidetes significantly modulates HF-induced glucose intolerance but has limited impact on obesity in mice. Our results suggest that gut microbiota is a part of complex aetiology of insulin resistance syndrome, individual microbiota composition may cause phenotypic variation associated with HF feeding in mice. Nature Publishing Group 2016-08-31 /pmc/articles/PMC5006052/ /pubmed/27577172 http://dx.doi.org/10.1038/srep32484 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Rabot, Sylvie
Membrez, Mathieu
Blancher, Florence
Berger, Bernard
Moine, Déborah
Krause, Lutz
Bibiloni, Rodrigo
Bruneau, Aurélia
Gérard, Philippe
Siddharth, Jay
Lauber, Christian L.
Chou, Chieh Jason
High fat diet drives obesity regardless the composition of gut microbiota in mice
title High fat diet drives obesity regardless the composition of gut microbiota in mice
title_full High fat diet drives obesity regardless the composition of gut microbiota in mice
title_fullStr High fat diet drives obesity regardless the composition of gut microbiota in mice
title_full_unstemmed High fat diet drives obesity regardless the composition of gut microbiota in mice
title_short High fat diet drives obesity regardless the composition of gut microbiota in mice
title_sort high fat diet drives obesity regardless the composition of gut microbiota in mice
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5006052/
https://www.ncbi.nlm.nih.gov/pubmed/27577172
http://dx.doi.org/10.1038/srep32484
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