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Electroacupuncture reduces blood glucose by regulating intestinal flora in type 2 diabetic mice

BACKGROUND: The development of diabetes is closely related to the gut microbiota in recent studies, which can be influenced by intestinal motility. A few studies report that electroacupuncture (EA) can lower blood glucose. EA can promote colonic motility and influence gut microbes. In this study, we...

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Autores principales: An, Jing, Wang, Lingli, Song, Shuangning, Tian, Lugao, Liu, Qingqing, Mei, Minhui, Li, Wenhua, Liu, Shi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wiley Publishing Asia Pty Ltd 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9574722/
https://www.ncbi.nlm.nih.gov/pubmed/36195536
http://dx.doi.org/10.1111/1753-0407.13323
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author An, Jing
Wang, Lingli
Song, Shuangning
Tian, Lugao
Liu, Qingqing
Mei, Minhui
Li, Wenhua
Liu, Shi
author_facet An, Jing
Wang, Lingli
Song, Shuangning
Tian, Lugao
Liu, Qingqing
Mei, Minhui
Li, Wenhua
Liu, Shi
author_sort An, Jing
collection PubMed
description BACKGROUND: The development of diabetes is closely related to the gut microbiota in recent studies, which can be influenced by intestinal motility. A few studies report that electroacupuncture (EA) can lower blood glucose. EA can promote colonic motility and influence gut microbes. In this study, we explored the effect of the EA on blood glucose level in mice with type 2 diabetes (T2D) and its mechanism. METHODS: The T2D mice model, fecal microbiota transplantation mice model, and Kit(W/Wv) mice model (Point mutation of mouse W locus encoding kit gene)were used to investigate the effect of EA on blood glucose as well as the mechanism; The blood glucose and insulin resistance level and the intestinal flora were evaluated. The level of intestinal junction protein, inflammatory cytokines in the serum, interstitial cells of Cajal content, and colonic motility were detected. Lastly, the IKKβ/NF‐κB‐JNK‐IRS‐1‐AKT pathway was explored. RESULTS: EA lowered the blood glucose level, altered the gut microbiota, and promoted colonic motility in T2D mice. EA‐altered microbiota decreased the blood glucose level and insulin resistance in the antibiotics‐treated diabetic mice. EA increased tight junction protein, lowered inflammatory factors, and regulated the IKKβ/NF‐κB‐JNK‐IRS‐1‐AKT pathway in the liver and muscles. EA could not reduce the blood glucose and regulated gut microbiota in the Kit(W/Wv) mice model. CONCLUSIONS: EA promoted intestinal motility to regulate the intestinal flora, thereby reducing the level of systemic inflammation, and ultimately lowering the blood glucose by the IKKβ/NF‐κB‐JNK‐IRS‐1‐AKT signal pathway.
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spelling pubmed-95747222022-10-17 Electroacupuncture reduces blood glucose by regulating intestinal flora in type 2 diabetic mice An, Jing Wang, Lingli Song, Shuangning Tian, Lugao Liu, Qingqing Mei, Minhui Li, Wenhua Liu, Shi J Diabetes Original Articles BACKGROUND: The development of diabetes is closely related to the gut microbiota in recent studies, which can be influenced by intestinal motility. A few studies report that electroacupuncture (EA) can lower blood glucose. EA can promote colonic motility and influence gut microbes. In this study, we explored the effect of the EA on blood glucose level in mice with type 2 diabetes (T2D) and its mechanism. METHODS: The T2D mice model, fecal microbiota transplantation mice model, and Kit(W/Wv) mice model (Point mutation of mouse W locus encoding kit gene)were used to investigate the effect of EA on blood glucose as well as the mechanism; The blood glucose and insulin resistance level and the intestinal flora were evaluated. The level of intestinal junction protein, inflammatory cytokines in the serum, interstitial cells of Cajal content, and colonic motility were detected. Lastly, the IKKβ/NF‐κB‐JNK‐IRS‐1‐AKT pathway was explored. RESULTS: EA lowered the blood glucose level, altered the gut microbiota, and promoted colonic motility in T2D mice. EA‐altered microbiota decreased the blood glucose level and insulin resistance in the antibiotics‐treated diabetic mice. EA increased tight junction protein, lowered inflammatory factors, and regulated the IKKβ/NF‐κB‐JNK‐IRS‐1‐AKT pathway in the liver and muscles. EA could not reduce the blood glucose and regulated gut microbiota in the Kit(W/Wv) mice model. CONCLUSIONS: EA promoted intestinal motility to regulate the intestinal flora, thereby reducing the level of systemic inflammation, and ultimately lowering the blood glucose by the IKKβ/NF‐κB‐JNK‐IRS‐1‐AKT signal pathway. Wiley Publishing Asia Pty Ltd 2022-10-04 /pmc/articles/PMC9574722/ /pubmed/36195536 http://dx.doi.org/10.1111/1753-0407.13323 Text en © 2022 The Authors. Journal of Diabetes published by Ruijin Hospital, Shanghai JiaoTong University School of Medicine and John Wiley & Sons Australia, Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
An, Jing
Wang, Lingli
Song, Shuangning
Tian, Lugao
Liu, Qingqing
Mei, Minhui
Li, Wenhua
Liu, Shi
Electroacupuncture reduces blood glucose by regulating intestinal flora in type 2 diabetic mice
title Electroacupuncture reduces blood glucose by regulating intestinal flora in type 2 diabetic mice
title_full Electroacupuncture reduces blood glucose by regulating intestinal flora in type 2 diabetic mice
title_fullStr Electroacupuncture reduces blood glucose by regulating intestinal flora in type 2 diabetic mice
title_full_unstemmed Electroacupuncture reduces blood glucose by regulating intestinal flora in type 2 diabetic mice
title_short Electroacupuncture reduces blood glucose by regulating intestinal flora in type 2 diabetic mice
title_sort electroacupuncture reduces blood glucose by regulating intestinal flora in type 2 diabetic mice
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9574722/
https://www.ncbi.nlm.nih.gov/pubmed/36195536
http://dx.doi.org/10.1111/1753-0407.13323
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