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Alleviation of high fat diet‐induced obesity by oligofructose in gnotobiotic mice is independent of presence of Bifidobacterium longum
SCOPE: Diet‐induced obesity is associated with changes in the gut microbiota and low‐grade inflammation. Oligofructose was reported to ameliorate high fat diet‐induced metabolic disorders in mice by restoring the number of intestinal bifidobacteria. However, this has not been experimentally demonstr...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5049449/ https://www.ncbi.nlm.nih.gov/pubmed/26202344 http://dx.doi.org/10.1002/mnfr.201500249 |
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author | Woting, Anni Pfeiffer, Nora Hanske, Laura Loh, Gunnar Klaus, Susanne Blaut, Michael |
author_facet | Woting, Anni Pfeiffer, Nora Hanske, Laura Loh, Gunnar Klaus, Susanne Blaut, Michael |
author_sort | Woting, Anni |
collection | PubMed |
description | SCOPE: Diet‐induced obesity is associated with changes in the gut microbiota and low‐grade inflammation. Oligofructose was reported to ameliorate high fat diet‐induced metabolic disorders in mice by restoring the number of intestinal bifidobacteria. However, this has not been experimentally demonstrated. METHODS AND RESULTS: We fed conventional mice, germfree mice, mice associated with a simplified human gut microbiota composed of eight bacterial species including Bifidobacterium longum (SIHUMI), and mice associated with SIHUMI without B. longum a low fat diet (LFD), a high fat diet (HFD), or a HFD containing 10% oligofructose (HFD + OFS) for five weeks. We assessed body composition, bacterial cell numbers and metabolites, markers of inflammation, and gut permeability. Conventional mice fed HFD or HFD + OFS did not differ in body weight gain and glucose tolerance. The gnotobiotic mouse groups fed LFD or HFD + OFS gained less body weight and body fat, and displayed an improved glucose tolerance compared with mice fed HFD. These differences were not affected by the presence of B. longum. Mice fed HFD showed no signs of inflammation or increased intestinal permeability. CONCLUSION: The ability of oligofructose to reduce obesity and to improve glucose tolerance in gnotobiotic mice fed HFD was independent of the presence of B. longum. |
format | Online Article Text |
id | pubmed-5049449 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-50494492016-10-06 Alleviation of high fat diet‐induced obesity by oligofructose in gnotobiotic mice is independent of presence of Bifidobacterium longum Woting, Anni Pfeiffer, Nora Hanske, Laura Loh, Gunnar Klaus, Susanne Blaut, Michael Mol Nutr Food Res Research Articles SCOPE: Diet‐induced obesity is associated with changes in the gut microbiota and low‐grade inflammation. Oligofructose was reported to ameliorate high fat diet‐induced metabolic disorders in mice by restoring the number of intestinal bifidobacteria. However, this has not been experimentally demonstrated. METHODS AND RESULTS: We fed conventional mice, germfree mice, mice associated with a simplified human gut microbiota composed of eight bacterial species including Bifidobacterium longum (SIHUMI), and mice associated with SIHUMI without B. longum a low fat diet (LFD), a high fat diet (HFD), or a HFD containing 10% oligofructose (HFD + OFS) for five weeks. We assessed body composition, bacterial cell numbers and metabolites, markers of inflammation, and gut permeability. Conventional mice fed HFD or HFD + OFS did not differ in body weight gain and glucose tolerance. The gnotobiotic mouse groups fed LFD or HFD + OFS gained less body weight and body fat, and displayed an improved glucose tolerance compared with mice fed HFD. These differences were not affected by the presence of B. longum. Mice fed HFD showed no signs of inflammation or increased intestinal permeability. CONCLUSION: The ability of oligofructose to reduce obesity and to improve glucose tolerance in gnotobiotic mice fed HFD was independent of the presence of B. longum. John Wiley and Sons Inc. 2015-08-26 2015-11 /pmc/articles/PMC5049449/ /pubmed/26202344 http://dx.doi.org/10.1002/mnfr.201500249 Text en © 2015 The Authors. Molecular Nutrition & Food Research published by Wiley‐VCH Verlag GmbH & Co. KGaA, Weinheim. This is an open access article under the terms of the Creative Commons Attribution‐Non‐Commercial‐NoDerivs (http://creativecommons.org/licenses/by-nc-nd/4.0/) Licence, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Research Articles Woting, Anni Pfeiffer, Nora Hanske, Laura Loh, Gunnar Klaus, Susanne Blaut, Michael Alleviation of high fat diet‐induced obesity by oligofructose in gnotobiotic mice is independent of presence of Bifidobacterium longum |
title | Alleviation of high fat diet‐induced obesity by oligofructose in gnotobiotic mice is independent of presence of Bifidobacterium longum
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title_full | Alleviation of high fat diet‐induced obesity by oligofructose in gnotobiotic mice is independent of presence of Bifidobacterium longum
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title_fullStr | Alleviation of high fat diet‐induced obesity by oligofructose in gnotobiotic mice is independent of presence of Bifidobacterium longum
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title_full_unstemmed | Alleviation of high fat diet‐induced obesity by oligofructose in gnotobiotic mice is independent of presence of Bifidobacterium longum
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title_short | Alleviation of high fat diet‐induced obesity by oligofructose in gnotobiotic mice is independent of presence of Bifidobacterium longum
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title_sort | alleviation of high fat diet‐induced obesity by oligofructose in gnotobiotic mice is independent of presence of bifidobacterium longum |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5049449/ https://www.ncbi.nlm.nih.gov/pubmed/26202344 http://dx.doi.org/10.1002/mnfr.201500249 |
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