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Roux-en-Y Gastric Bypass Improved Insulin Resistance via Alteration of the Human Gut Microbiome and Alleviation of Endotoxemia

BACKGROUND: Obesity is a main contributing factor for the development of glucose intolerance and type 2 diabetes mellitus (T2D). Roux-en-Y gastric bypass (RYGB) is believed to be one of the most effective treatments to reduce body weight and improve glucose metabolism. In this study, we sought to ex...

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Autores principales: Shi, Qiping, Wang, Qian, Zhong, Hui, Li, Dehai, Yu, Shuxing, Yang, Hengwen, Wang, Cunchuan, Yin, Zhinan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8294027/
https://www.ncbi.nlm.nih.gov/pubmed/34337024
http://dx.doi.org/10.1155/2021/5554991
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author Shi, Qiping
Wang, Qian
Zhong, Hui
Li, Dehai
Yu, Shuxing
Yang, Hengwen
Wang, Cunchuan
Yin, Zhinan
author_facet Shi, Qiping
Wang, Qian
Zhong, Hui
Li, Dehai
Yu, Shuxing
Yang, Hengwen
Wang, Cunchuan
Yin, Zhinan
author_sort Shi, Qiping
collection PubMed
description BACKGROUND: Obesity is a main contributing factor for the development of glucose intolerance and type 2 diabetes mellitus (T2D). Roux-en-Y gastric bypass (RYGB) is believed to be one of the most effective treatments to reduce body weight and improve glucose metabolism. In this study, we sought to explore the underlying mechanisms of weight reduction and insulin resistance improvement after RYGB. METHODS: This was a prospective observational study using consecutive samples of 14 obese subjects undergoing bariatric surgery. Main assessments were serum indexes (blood metabolites, glucose-lipid regulating hormones, trimethylamine-N-oxide (TMAO), and lipopolysaccharide-binding protein (LBP), fecal short-chain fatty acids (SCFAs), and gut microbiota. Correlation analysis of the factors changed by RYGB was used to indicate the potential mechanism by which surgery improves insulin resistance. RESULTS: The subjects showed significant improvement on indices of obesity and insulin resistance and a correlated change of gut microbiota components at 1 month, 3 months, and 6 months post-RYGB operation. In particular, the abundance of a counterobese strain, Akkemansia muciniphila, had gradually increased with the postoperative time. Moreover, these changes were negatively correlated to serum levels of LBP and positively correlated to serum TMAO and fecal SCFAs. CONCLUSIONS: Our findings uncovered links between intestinal microbiota alterations, circulating endotoxemia, and insulin resistance. This suggests that the underlying mechanism of protection of the intestine by RYGB in obesity may be through changing the gut microbiota.
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spelling pubmed-82940272021-07-31 Roux-en-Y Gastric Bypass Improved Insulin Resistance via Alteration of the Human Gut Microbiome and Alleviation of Endotoxemia Shi, Qiping Wang, Qian Zhong, Hui Li, Dehai Yu, Shuxing Yang, Hengwen Wang, Cunchuan Yin, Zhinan Biomed Res Int Research Article BACKGROUND: Obesity is a main contributing factor for the development of glucose intolerance and type 2 diabetes mellitus (T2D). Roux-en-Y gastric bypass (RYGB) is believed to be one of the most effective treatments to reduce body weight and improve glucose metabolism. In this study, we sought to explore the underlying mechanisms of weight reduction and insulin resistance improvement after RYGB. METHODS: This was a prospective observational study using consecutive samples of 14 obese subjects undergoing bariatric surgery. Main assessments were serum indexes (blood metabolites, glucose-lipid regulating hormones, trimethylamine-N-oxide (TMAO), and lipopolysaccharide-binding protein (LBP), fecal short-chain fatty acids (SCFAs), and gut microbiota. Correlation analysis of the factors changed by RYGB was used to indicate the potential mechanism by which surgery improves insulin resistance. RESULTS: The subjects showed significant improvement on indices of obesity and insulin resistance and a correlated change of gut microbiota components at 1 month, 3 months, and 6 months post-RYGB operation. In particular, the abundance of a counterobese strain, Akkemansia muciniphila, had gradually increased with the postoperative time. Moreover, these changes were negatively correlated to serum levels of LBP and positively correlated to serum TMAO and fecal SCFAs. CONCLUSIONS: Our findings uncovered links between intestinal microbiota alterations, circulating endotoxemia, and insulin resistance. This suggests that the underlying mechanism of protection of the intestine by RYGB in obesity may be through changing the gut microbiota. Hindawi 2021-07-12 /pmc/articles/PMC8294027/ /pubmed/34337024 http://dx.doi.org/10.1155/2021/5554991 Text en Copyright © 2021 Qiping Shi et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Shi, Qiping
Wang, Qian
Zhong, Hui
Li, Dehai
Yu, Shuxing
Yang, Hengwen
Wang, Cunchuan
Yin, Zhinan
Roux-en-Y Gastric Bypass Improved Insulin Resistance via Alteration of the Human Gut Microbiome and Alleviation of Endotoxemia
title Roux-en-Y Gastric Bypass Improved Insulin Resistance via Alteration of the Human Gut Microbiome and Alleviation of Endotoxemia
title_full Roux-en-Y Gastric Bypass Improved Insulin Resistance via Alteration of the Human Gut Microbiome and Alleviation of Endotoxemia
title_fullStr Roux-en-Y Gastric Bypass Improved Insulin Resistance via Alteration of the Human Gut Microbiome and Alleviation of Endotoxemia
title_full_unstemmed Roux-en-Y Gastric Bypass Improved Insulin Resistance via Alteration of the Human Gut Microbiome and Alleviation of Endotoxemia
title_short Roux-en-Y Gastric Bypass Improved Insulin Resistance via Alteration of the Human Gut Microbiome and Alleviation of Endotoxemia
title_sort roux-en-y gastric bypass improved insulin resistance via alteration of the human gut microbiome and alleviation of endotoxemia
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8294027/
https://www.ncbi.nlm.nih.gov/pubmed/34337024
http://dx.doi.org/10.1155/2021/5554991
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