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Dysbiosis of intestinal microbiota in early life aggravates high-fat diet induced dysmetabolism in adult mice

BACKGROUND: Accumulating evidence have shown that the intestinal microbiota plays an important role in prevention of host obesity and metabolism disorders. Recent studies also demonstrate that early life is the key time for the colonization of intestinal microbes in host. However, there are few stud...

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Autores principales: Miao, Z. H., Zhou, W. X., Cheng, R. Y., Liang, H. J., Jiang, F. L., Shen, X., Lu, J. H., Li, M., He, F.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8268513/
https://www.ncbi.nlm.nih.gov/pubmed/34238228
http://dx.doi.org/10.1186/s12866-021-02263-6
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author Miao, Z. H.
Zhou, W. X.
Cheng, R. Y.
Liang, H. J.
Jiang, F. L.
Shen, X.
Lu, J. H.
Li, M.
He, F.
author_facet Miao, Z. H.
Zhou, W. X.
Cheng, R. Y.
Liang, H. J.
Jiang, F. L.
Shen, X.
Lu, J. H.
Li, M.
He, F.
author_sort Miao, Z. H.
collection PubMed
description BACKGROUND: Accumulating evidence have shown that the intestinal microbiota plays an important role in prevention of host obesity and metabolism disorders. Recent studies also demonstrate that early life is the key time for the colonization of intestinal microbes in host. However, there are few studies focusing on possible association between intestinal microbiota in the early life and metabolism in adulthood. Therefore the present study was conducted to examine whether the short term antibiotic and/or probiotic exposure in early life could affect intestinal microbes and their possible long term effects on host metabolism. RESULTS: A high-fat diet resulted in glucose and lipid metabolism disorders with higher levels of visceral fat rate, insulin-resistance indices, and leptin. Exposure to ceftriaxone in early life aggravated the negative influences of a high-fat diet on mouse physiology. Orally fed TMC3115 protected mice, especially those who had received treatment throughout the whole study, from damage due to a high-fat diet, such as increases in levels of fasting blood glucose and serum levels of insulin, leptin, and IR indices. Exposure to ceftriaxone during the first 2 weeks of life was linked to dysbiosis of the fecal microbiota with a significant decrease in the species richness and diversity. However, the influence of orally fed ceftriaxone on the fecal microbiota was limited to 12 weeks after the termination of treatment. Of note, at week 12 there were still some differences in the composition of intestinal microbiota between mice provided with high fat diet and antibiotic exposure and those only fed a high fat diet. CONCLUSIONS: These results indicated that exposure to antibiotics, such as ceftriaxone, in early life may aggravate the negative influences of a high-fat diet on the physiology of the host animal. These results also suggest that the crosstalk between the host and their intestinal microbiota in early life may be more important than that in adulthood, even though the same intestinal microbes are present in adulthood. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-021-02263-6.
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spelling pubmed-82685132021-07-09 Dysbiosis of intestinal microbiota in early life aggravates high-fat diet induced dysmetabolism in adult mice Miao, Z. H. Zhou, W. X. Cheng, R. Y. Liang, H. J. Jiang, F. L. Shen, X. Lu, J. H. Li, M. He, F. BMC Microbiol Research Article BACKGROUND: Accumulating evidence have shown that the intestinal microbiota plays an important role in prevention of host obesity and metabolism disorders. Recent studies also demonstrate that early life is the key time for the colonization of intestinal microbes in host. However, there are few studies focusing on possible association between intestinal microbiota in the early life and metabolism in adulthood. Therefore the present study was conducted to examine whether the short term antibiotic and/or probiotic exposure in early life could affect intestinal microbes and their possible long term effects on host metabolism. RESULTS: A high-fat diet resulted in glucose and lipid metabolism disorders with higher levels of visceral fat rate, insulin-resistance indices, and leptin. Exposure to ceftriaxone in early life aggravated the negative influences of a high-fat diet on mouse physiology. Orally fed TMC3115 protected mice, especially those who had received treatment throughout the whole study, from damage due to a high-fat diet, such as increases in levels of fasting blood glucose and serum levels of insulin, leptin, and IR indices. Exposure to ceftriaxone during the first 2 weeks of life was linked to dysbiosis of the fecal microbiota with a significant decrease in the species richness and diversity. However, the influence of orally fed ceftriaxone on the fecal microbiota was limited to 12 weeks after the termination of treatment. Of note, at week 12 there were still some differences in the composition of intestinal microbiota between mice provided with high fat diet and antibiotic exposure and those only fed a high fat diet. CONCLUSIONS: These results indicated that exposure to antibiotics, such as ceftriaxone, in early life may aggravate the negative influences of a high-fat diet on the physiology of the host animal. These results also suggest that the crosstalk between the host and their intestinal microbiota in early life may be more important than that in adulthood, even though the same intestinal microbes are present in adulthood. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-021-02263-6. BioMed Central 2021-07-08 /pmc/articles/PMC8268513/ /pubmed/34238228 http://dx.doi.org/10.1186/s12866-021-02263-6 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research Article
Miao, Z. H.
Zhou, W. X.
Cheng, R. Y.
Liang, H. J.
Jiang, F. L.
Shen, X.
Lu, J. H.
Li, M.
He, F.
Dysbiosis of intestinal microbiota in early life aggravates high-fat diet induced dysmetabolism in adult mice
title Dysbiosis of intestinal microbiota in early life aggravates high-fat diet induced dysmetabolism in adult mice
title_full Dysbiosis of intestinal microbiota in early life aggravates high-fat diet induced dysmetabolism in adult mice
title_fullStr Dysbiosis of intestinal microbiota in early life aggravates high-fat diet induced dysmetabolism in adult mice
title_full_unstemmed Dysbiosis of intestinal microbiota in early life aggravates high-fat diet induced dysmetabolism in adult mice
title_short Dysbiosis of intestinal microbiota in early life aggravates high-fat diet induced dysmetabolism in adult mice
title_sort dysbiosis of intestinal microbiota in early life aggravates high-fat diet induced dysmetabolism in adult mice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8268513/
https://www.ncbi.nlm.nih.gov/pubmed/34238228
http://dx.doi.org/10.1186/s12866-021-02263-6
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