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Perturbation on gut microbiota impedes the onset of obesity in high fat diet-induced mice
High-calorie intake has become one of the most common causes of dietary obesity, which eventually develops into type 2 diabetes mellitus (T2DM). Microbiota, along with the length of the gastrointestinal tract, is related to metabolic disorders, but its shifts and following impact on metabolic disord...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9395671/ https://www.ncbi.nlm.nih.gov/pubmed/36017311 http://dx.doi.org/10.3389/fendo.2022.795371 |
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author | Yu, Zhongjia Yu, Xiang-Fang Kerem, Goher Ren, Pei-Gen |
author_facet | Yu, Zhongjia Yu, Xiang-Fang Kerem, Goher Ren, Pei-Gen |
author_sort | Yu, Zhongjia |
collection | PubMed |
description | High-calorie intake has become one of the most common causes of dietary obesity, which eventually develops into type 2 diabetes mellitus (T2DM). Microbiota, along with the length of the gastrointestinal tract, is related to metabolic disorders, but its shifts and following impact on metabolic disorders due to external perturbation are still unclear. To evaluate shifts of microbiota from the proximal to the distal intestine and their impact on metabolic disorders, we profiled jejunal and colonic microbiota with the perturbation using high salt (HS) and antibiotic-induced microbiota depletion (AIMD) in diet-induced obesity (DIO) mice and analyzed the association with parameters of both obesity and blood glucose. After ten weeks of feeding DIO mice with HS intake and AIMD, they failed to develop obesity. The DIO mice with HS intake had T2DM symptoms, whereas the AIMD DIO mice showed no significant difference in blood glucose parameters. We observed that the jejunal and colonic microbiota had shifted due to settled perturbation, and jejunal microbiota within a group were more dispersed than colonic microbiota. After further analyzing jejunal microbiota using quantified amplicon sequencing, we found that the absolute abundance of Colidextribacter (R = 0.695, p = 0.001) and Faecalibaculum (R = 0.631, p = 0.005) in the jejunum was positively correlated with the changes in BW and FBG levels. The predicted pathway of glucose and metabolism of other substances significantly changed between groups (p <0.05). We demonstrated that the onset of obesity and T2DM in DIO mice is impeded when the gut microbiota is perturbed; thus, this pathogenesis depends on the gut microbiota. |
format | Online Article Text |
id | pubmed-9395671 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-93956712022-08-24 Perturbation on gut microbiota impedes the onset of obesity in high fat diet-induced mice Yu, Zhongjia Yu, Xiang-Fang Kerem, Goher Ren, Pei-Gen Front Endocrinol (Lausanne) Endocrinology High-calorie intake has become one of the most common causes of dietary obesity, which eventually develops into type 2 diabetes mellitus (T2DM). Microbiota, along with the length of the gastrointestinal tract, is related to metabolic disorders, but its shifts and following impact on metabolic disorders due to external perturbation are still unclear. To evaluate shifts of microbiota from the proximal to the distal intestine and their impact on metabolic disorders, we profiled jejunal and colonic microbiota with the perturbation using high salt (HS) and antibiotic-induced microbiota depletion (AIMD) in diet-induced obesity (DIO) mice and analyzed the association with parameters of both obesity and blood glucose. After ten weeks of feeding DIO mice with HS intake and AIMD, they failed to develop obesity. The DIO mice with HS intake had T2DM symptoms, whereas the AIMD DIO mice showed no significant difference in blood glucose parameters. We observed that the jejunal and colonic microbiota had shifted due to settled perturbation, and jejunal microbiota within a group were more dispersed than colonic microbiota. After further analyzing jejunal microbiota using quantified amplicon sequencing, we found that the absolute abundance of Colidextribacter (R = 0.695, p = 0.001) and Faecalibaculum (R = 0.631, p = 0.005) in the jejunum was positively correlated with the changes in BW and FBG levels. The predicted pathway of glucose and metabolism of other substances significantly changed between groups (p <0.05). We demonstrated that the onset of obesity and T2DM in DIO mice is impeded when the gut microbiota is perturbed; thus, this pathogenesis depends on the gut microbiota. Frontiers Media S.A. 2022-08-09 /pmc/articles/PMC9395671/ /pubmed/36017311 http://dx.doi.org/10.3389/fendo.2022.795371 Text en Copyright © 2022 Yu, Yu, Kerem and Ren https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Endocrinology Yu, Zhongjia Yu, Xiang-Fang Kerem, Goher Ren, Pei-Gen Perturbation on gut microbiota impedes the onset of obesity in high fat diet-induced mice |
title | Perturbation on gut microbiota impedes the onset of obesity in high fat diet-induced mice |
title_full | Perturbation on gut microbiota impedes the onset of obesity in high fat diet-induced mice |
title_fullStr | Perturbation on gut microbiota impedes the onset of obesity in high fat diet-induced mice |
title_full_unstemmed | Perturbation on gut microbiota impedes the onset of obesity in high fat diet-induced mice |
title_short | Perturbation on gut microbiota impedes the onset of obesity in high fat diet-induced mice |
title_sort | perturbation on gut microbiota impedes the onset of obesity in high fat diet-induced mice |
topic | Endocrinology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9395671/ https://www.ncbi.nlm.nih.gov/pubmed/36017311 http://dx.doi.org/10.3389/fendo.2022.795371 |
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