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Gut microbe-derived extracellular vesicles induce insulin resistance, thereby impairing glucose metabolism in skeletal muscle

Gut microbes might influence host metabolic homeostasis and contribute to the pathogenesis of type 2 diabetes (T2D), which is characterized by insulin resistance. Bacteria-derived extracellular vesicles (EVs) have been suggested to be important in the pathogenesis of diseases once believed to be non...

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Autores principales: Choi, Youngwoo, Kwon, Yonghoon, Kim, Dae-Kyum, Jeon, Jinseong, Jang, Su Chul, Wang, Taejun, Ban, Minjee, Kim, Min-Hye, Jeon, Seong Gyu, Kim, Min-Sun, Choi, Cheol Soo, Jee, Young-Koo, Gho, Yong Song, Ryu, Sung Ho, Kim, Yoon-Keun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4625370/
https://www.ncbi.nlm.nih.gov/pubmed/26510393
http://dx.doi.org/10.1038/srep15878
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author Choi, Youngwoo
Kwon, Yonghoon
Kim, Dae-Kyum
Jeon, Jinseong
Jang, Su Chul
Wang, Taejun
Ban, Minjee
Kim, Min-Hye
Jeon, Seong Gyu
Kim, Min-Sun
Choi, Cheol Soo
Jee, Young-Koo
Gho, Yong Song
Ryu, Sung Ho
Kim, Yoon-Keun
author_facet Choi, Youngwoo
Kwon, Yonghoon
Kim, Dae-Kyum
Jeon, Jinseong
Jang, Su Chul
Wang, Taejun
Ban, Minjee
Kim, Min-Hye
Jeon, Seong Gyu
Kim, Min-Sun
Choi, Cheol Soo
Jee, Young-Koo
Gho, Yong Song
Ryu, Sung Ho
Kim, Yoon-Keun
author_sort Choi, Youngwoo
collection PubMed
description Gut microbes might influence host metabolic homeostasis and contribute to the pathogenesis of type 2 diabetes (T2D), which is characterized by insulin resistance. Bacteria-derived extracellular vesicles (EVs) have been suggested to be important in the pathogenesis of diseases once believed to be non-infectious. Here, we hypothesize that gut microbe-derived EVs are important in the pathogenesis of T2D. In vivo administration of stool EVs from high fat diet (HFD)-fed mice induced insulin resistance and glucose intolerance compared to regular diet (RD)-fed mice. Metagenomic profiling of stool EVs by 16S ribosomal DNA sequencing revealed an increased amount of EVs derived from Pseudomonas panacis (phylum Proteobacteria) in HFD mice compared to RD mice. Interestingly, P. panacis EVs blocked the insulin signaling pathway in both skeletal muscle and adipose tissue. Moreover, isolated P. panacis EVs induced typical diabetic phenotypes, such as glucose intolerance after glucose administration or systemic insulin injection. Thus, gut microbe-derived EVs might be key players in the development of insulin resistance and impairment of glucose metabolism promoted by HFD.
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spelling pubmed-46253702015-11-03 Gut microbe-derived extracellular vesicles induce insulin resistance, thereby impairing glucose metabolism in skeletal muscle Choi, Youngwoo Kwon, Yonghoon Kim, Dae-Kyum Jeon, Jinseong Jang, Su Chul Wang, Taejun Ban, Minjee Kim, Min-Hye Jeon, Seong Gyu Kim, Min-Sun Choi, Cheol Soo Jee, Young-Koo Gho, Yong Song Ryu, Sung Ho Kim, Yoon-Keun Sci Rep Article Gut microbes might influence host metabolic homeostasis and contribute to the pathogenesis of type 2 diabetes (T2D), which is characterized by insulin resistance. Bacteria-derived extracellular vesicles (EVs) have been suggested to be important in the pathogenesis of diseases once believed to be non-infectious. Here, we hypothesize that gut microbe-derived EVs are important in the pathogenesis of T2D. In vivo administration of stool EVs from high fat diet (HFD)-fed mice induced insulin resistance and glucose intolerance compared to regular diet (RD)-fed mice. Metagenomic profiling of stool EVs by 16S ribosomal DNA sequencing revealed an increased amount of EVs derived from Pseudomonas panacis (phylum Proteobacteria) in HFD mice compared to RD mice. Interestingly, P. panacis EVs blocked the insulin signaling pathway in both skeletal muscle and adipose tissue. Moreover, isolated P. panacis EVs induced typical diabetic phenotypes, such as glucose intolerance after glucose administration or systemic insulin injection. Thus, gut microbe-derived EVs might be key players in the development of insulin resistance and impairment of glucose metabolism promoted by HFD. Nature Publishing Group 2015-10-29 /pmc/articles/PMC4625370/ /pubmed/26510393 http://dx.doi.org/10.1038/srep15878 Text en Copyright © 2015, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Choi, Youngwoo
Kwon, Yonghoon
Kim, Dae-Kyum
Jeon, Jinseong
Jang, Su Chul
Wang, Taejun
Ban, Minjee
Kim, Min-Hye
Jeon, Seong Gyu
Kim, Min-Sun
Choi, Cheol Soo
Jee, Young-Koo
Gho, Yong Song
Ryu, Sung Ho
Kim, Yoon-Keun
Gut microbe-derived extracellular vesicles induce insulin resistance, thereby impairing glucose metabolism in skeletal muscle
title Gut microbe-derived extracellular vesicles induce insulin resistance, thereby impairing glucose metabolism in skeletal muscle
title_full Gut microbe-derived extracellular vesicles induce insulin resistance, thereby impairing glucose metabolism in skeletal muscle
title_fullStr Gut microbe-derived extracellular vesicles induce insulin resistance, thereby impairing glucose metabolism in skeletal muscle
title_full_unstemmed Gut microbe-derived extracellular vesicles induce insulin resistance, thereby impairing glucose metabolism in skeletal muscle
title_short Gut microbe-derived extracellular vesicles induce insulin resistance, thereby impairing glucose metabolism in skeletal muscle
title_sort gut microbe-derived extracellular vesicles induce insulin resistance, thereby impairing glucose metabolism in skeletal muscle
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4625370/
https://www.ncbi.nlm.nih.gov/pubmed/26510393
http://dx.doi.org/10.1038/srep15878
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