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Mechanisms linking gut microbial metabolites to insulin resistance

Insulin resistance is the rate-limiting step in the development of metabolic diseases, including type 2 diabetes. The gut microbiota has been implicated in host energy metabolism and metabolic diseases and is recognized as a quantitatively important organelle in host metabolism, as the human gut har...

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Detalles Bibliográficos
Autores principales: Jang, Hye Rim, Lee, Hui-Young
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Baishideng Publishing Group Inc 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8192250/
https://www.ncbi.nlm.nih.gov/pubmed/34168724
http://dx.doi.org/10.4239/wjd.v12.i6.730
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author Jang, Hye Rim
Lee, Hui-Young
author_facet Jang, Hye Rim
Lee, Hui-Young
author_sort Jang, Hye Rim
collection PubMed
description Insulin resistance is the rate-limiting step in the development of metabolic diseases, including type 2 diabetes. The gut microbiota has been implicated in host energy metabolism and metabolic diseases and is recognized as a quantitatively important organelle in host metabolism, as the human gut harbors 10 trillion bacterial cells. Gut microbiota break down various nutrients and produce metabolites that play fundamental roles in host metabolism and aid in the identification of possible therapeutic targets for metabolic diseases. Therefore, understanding the various effects of bacterial metabolites in the development of insulin resistance is critical. Here, we review the mechanisms linking gut microbial metabolites to insulin resistance in various insulin-responsive tissues.
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spelling pubmed-81922502021-06-23 Mechanisms linking gut microbial metabolites to insulin resistance Jang, Hye Rim Lee, Hui-Young World J Diabetes Review Insulin resistance is the rate-limiting step in the development of metabolic diseases, including type 2 diabetes. The gut microbiota has been implicated in host energy metabolism and metabolic diseases and is recognized as a quantitatively important organelle in host metabolism, as the human gut harbors 10 trillion bacterial cells. Gut microbiota break down various nutrients and produce metabolites that play fundamental roles in host metabolism and aid in the identification of possible therapeutic targets for metabolic diseases. Therefore, understanding the various effects of bacterial metabolites in the development of insulin resistance is critical. Here, we review the mechanisms linking gut microbial metabolites to insulin resistance in various insulin-responsive tissues. Baishideng Publishing Group Inc 2021-06-15 2021-06-15 /pmc/articles/PMC8192250/ /pubmed/34168724 http://dx.doi.org/10.4239/wjd.v12.i6.730 Text en ©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved. https://creativecommons.org/licenses/by-nc/4.0/This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
spellingShingle Review
Jang, Hye Rim
Lee, Hui-Young
Mechanisms linking gut microbial metabolites to insulin resistance
title Mechanisms linking gut microbial metabolites to insulin resistance
title_full Mechanisms linking gut microbial metabolites to insulin resistance
title_fullStr Mechanisms linking gut microbial metabolites to insulin resistance
title_full_unstemmed Mechanisms linking gut microbial metabolites to insulin resistance
title_short Mechanisms linking gut microbial metabolites to insulin resistance
title_sort mechanisms linking gut microbial metabolites to insulin resistance
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8192250/
https://www.ncbi.nlm.nih.gov/pubmed/34168724
http://dx.doi.org/10.4239/wjd.v12.i6.730
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