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Regulation of tartary buckwheat‐resistant starch on intestinal microflora in mice fed with high‐fat diet
Resistant starch (RS) is closely related to the composition of intestinal flora. Based on many studies on the physiological functions of probiotics and short‐chain fatty acids (SCFAs), it is possible that RS can improve the intestinal health of the host. Therefore, we speculated that tartary buckwhe...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7382121/ https://www.ncbi.nlm.nih.gov/pubmed/32724589 http://dx.doi.org/10.1002/fsn3.1601 |
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author | Zhou, Yiming Wei, Yun Yan, Beibei Zhao, Shen Zhou, Xiaoli |
author_facet | Zhou, Yiming Wei, Yun Yan, Beibei Zhao, Shen Zhou, Xiaoli |
author_sort | Zhou, Yiming |
collection | PubMed |
description | Resistant starch (RS) is closely related to the composition of intestinal flora. Based on many studies on the physiological functions of probiotics and short‐chain fatty acids (SCFAs), it is possible that RS can improve the intestinal health of the host. Therefore, we speculated that tartary buckwheat‐resistant starch (TBRS) can also regulate the intestinal flora disorder caused by high‐fat diet. We randomly divided 36 SPF C57BL/6J mice into low‐fat diet, high‐fat diet (HF‐CS), high‐fat diet supplemented with TBRS (HF‐BRS), and high‐fat diet supplemented with corn‐resistant starch (HF‐CRS). We analyzed the diversity and richness of gut microbiota based on PCR and Illumina high‐throughput sequencing technology. In community abundance, the HF‐BRS group was significantly higher than the other three groups (p < .05). TBRS improved the gut microbiota dysbiosis, including decreasing the Firmicutes‐to‐Bacteroidetes ratios (F/B) and contributing to the growth of Bacteroides and Blautia as well significantly inhibiting the growth of Bifidobacterium, Faecalibaculum, and Erysipelatoclostridium. We also analyzed the production of SCFAs by GC‐MS, and the concentration of total SCFAs increased in the HF‐CS group. However, TBRS significantly increased the production of SCFAs, especially the propionate concentration compared with the HF‐CRS group (p < .05). These results elucidated that TBRS has the potential to improve intestinal health by altering the structure of gut microbiota and increasing the production of SCFAs. Our findings have important implications for TBRS as functional food ingredient to manipulate intestinal microflora. |
format | Online Article Text |
id | pubmed-7382121 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-73821212020-07-27 Regulation of tartary buckwheat‐resistant starch on intestinal microflora in mice fed with high‐fat diet Zhou, Yiming Wei, Yun Yan, Beibei Zhao, Shen Zhou, Xiaoli Food Sci Nutr Original Research Resistant starch (RS) is closely related to the composition of intestinal flora. Based on many studies on the physiological functions of probiotics and short‐chain fatty acids (SCFAs), it is possible that RS can improve the intestinal health of the host. Therefore, we speculated that tartary buckwheat‐resistant starch (TBRS) can also regulate the intestinal flora disorder caused by high‐fat diet. We randomly divided 36 SPF C57BL/6J mice into low‐fat diet, high‐fat diet (HF‐CS), high‐fat diet supplemented with TBRS (HF‐BRS), and high‐fat diet supplemented with corn‐resistant starch (HF‐CRS). We analyzed the diversity and richness of gut microbiota based on PCR and Illumina high‐throughput sequencing technology. In community abundance, the HF‐BRS group was significantly higher than the other three groups (p < .05). TBRS improved the gut microbiota dysbiosis, including decreasing the Firmicutes‐to‐Bacteroidetes ratios (F/B) and contributing to the growth of Bacteroides and Blautia as well significantly inhibiting the growth of Bifidobacterium, Faecalibaculum, and Erysipelatoclostridium. We also analyzed the production of SCFAs by GC‐MS, and the concentration of total SCFAs increased in the HF‐CS group. However, TBRS significantly increased the production of SCFAs, especially the propionate concentration compared with the HF‐CRS group (p < .05). These results elucidated that TBRS has the potential to improve intestinal health by altering the structure of gut microbiota and increasing the production of SCFAs. Our findings have important implications for TBRS as functional food ingredient to manipulate intestinal microflora. John Wiley and Sons Inc. 2020-05-12 /pmc/articles/PMC7382121/ /pubmed/32724589 http://dx.doi.org/10.1002/fsn3.1601 Text en © 2020 The Authors. Food Science & Nutrition published by Wiley Periodicals LLC. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Zhou, Yiming Wei, Yun Yan, Beibei Zhao, Shen Zhou, Xiaoli Regulation of tartary buckwheat‐resistant starch on intestinal microflora in mice fed with high‐fat diet |
title | Regulation of tartary buckwheat‐resistant starch on intestinal microflora in mice fed with high‐fat diet |
title_full | Regulation of tartary buckwheat‐resistant starch on intestinal microflora in mice fed with high‐fat diet |
title_fullStr | Regulation of tartary buckwheat‐resistant starch on intestinal microflora in mice fed with high‐fat diet |
title_full_unstemmed | Regulation of tartary buckwheat‐resistant starch on intestinal microflora in mice fed with high‐fat diet |
title_short | Regulation of tartary buckwheat‐resistant starch on intestinal microflora in mice fed with high‐fat diet |
title_sort | regulation of tartary buckwheat‐resistant starch on intestinal microflora in mice fed with high‐fat diet |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7382121/ https://www.ncbi.nlm.nih.gov/pubmed/32724589 http://dx.doi.org/10.1002/fsn3.1601 |
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