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Cecal microbial transplantation attenuates hyperthyroid‐induced thermogenesis in Mongolian gerbils

Endothermic mammals have a high energy cost to maintain a stable and high body temperature (T(b) , around 37°C). Thyroid hormones are a major regulator for energy metabolism and T(b) . The gut microbiota is involved in modulating host energy metabolism. However, whether the interaction between the g...

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Autores principales: Khakisahneh, Saeid, Zhang, Xue‐Ying, Nouri, Zahra, Wang, De‐Hua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8913869/
https://www.ncbi.nlm.nih.gov/pubmed/33729663
http://dx.doi.org/10.1111/1751-7915.13793
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author Khakisahneh, Saeid
Zhang, Xue‐Ying
Nouri, Zahra
Wang, De‐Hua
author_facet Khakisahneh, Saeid
Zhang, Xue‐Ying
Nouri, Zahra
Wang, De‐Hua
author_sort Khakisahneh, Saeid
collection PubMed
description Endothermic mammals have a high energy cost to maintain a stable and high body temperature (T(b) , around 37°C). Thyroid hormones are a major regulator for energy metabolism and T(b) . The gut microbiota is involved in modulating host energy metabolism. However, whether the interaction between the gut microbiota and thyroid hormones is involved in metabolic and thermal regulations is unclear. We hypothesized that thyroid hormones via an interaction with gut microbiota orchestrate host thermogenesis and T(b) . l‐thyroxine‐induced hyperthyroid Mongolian gerbils (Meriones unguiculatus) increased resting metabolic rate (RMR) and T(b) , whereas Methimazole‐induced hypothyroid animals decreased RMR. Both hypothyroid and hyperthyroid animals differed significantly in faecal bacterial community. Hyperthyroidism increased the relative abundance of pathogenic bacteria, such as Helicobacter and Rikenella, and decreased abundance of beneficial bacteria Butyricimonas and Parabacteroides, accompanied by reduced total bile acids and short‐chain fatty acids. Furthermore, the hyperthyroid gerbils transplanted with the microbiota from control donors increased type 2 deiodinase (DIO2) expression in the liver and showed a greater rate of decline of both serum T3 and T4 levels and, consequently, a more rapid recovery of normal RMR and T(b) . These findings indicate that thyroid hormones regulate thermogenesis depending on gut microbiota and colonization with normal microbiota by caecal microbial transplantation attenuates hyperthyroid‐induced thermogenesis. This work reveals the functional consequences of the gut microbiota‐thyroid axis in controlling host metabolic physiology and T(b) in endotherms.
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spelling pubmed-89138692022-03-17 Cecal microbial transplantation attenuates hyperthyroid‐induced thermogenesis in Mongolian gerbils Khakisahneh, Saeid Zhang, Xue‐Ying Nouri, Zahra Wang, De‐Hua Microb Biotechnol Research Articles Endothermic mammals have a high energy cost to maintain a stable and high body temperature (T(b) , around 37°C). Thyroid hormones are a major regulator for energy metabolism and T(b) . The gut microbiota is involved in modulating host energy metabolism. However, whether the interaction between the gut microbiota and thyroid hormones is involved in metabolic and thermal regulations is unclear. We hypothesized that thyroid hormones via an interaction with gut microbiota orchestrate host thermogenesis and T(b) . l‐thyroxine‐induced hyperthyroid Mongolian gerbils (Meriones unguiculatus) increased resting metabolic rate (RMR) and T(b) , whereas Methimazole‐induced hypothyroid animals decreased RMR. Both hypothyroid and hyperthyroid animals differed significantly in faecal bacterial community. Hyperthyroidism increased the relative abundance of pathogenic bacteria, such as Helicobacter and Rikenella, and decreased abundance of beneficial bacteria Butyricimonas and Parabacteroides, accompanied by reduced total bile acids and short‐chain fatty acids. Furthermore, the hyperthyroid gerbils transplanted with the microbiota from control donors increased type 2 deiodinase (DIO2) expression in the liver and showed a greater rate of decline of both serum T3 and T4 levels and, consequently, a more rapid recovery of normal RMR and T(b) . These findings indicate that thyroid hormones regulate thermogenesis depending on gut microbiota and colonization with normal microbiota by caecal microbial transplantation attenuates hyperthyroid‐induced thermogenesis. This work reveals the functional consequences of the gut microbiota‐thyroid axis in controlling host metabolic physiology and T(b) in endotherms. John Wiley and Sons Inc. 2021-03-17 /pmc/articles/PMC8913869/ /pubmed/33729663 http://dx.doi.org/10.1111/1751-7915.13793 Text en © 2021 The Authors. Microbial Biotechnology published by John Wiley & Sons Ltd and Society for Applied Microbiology. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Research Articles
Khakisahneh, Saeid
Zhang, Xue‐Ying
Nouri, Zahra
Wang, De‐Hua
Cecal microbial transplantation attenuates hyperthyroid‐induced thermogenesis in Mongolian gerbils
title Cecal microbial transplantation attenuates hyperthyroid‐induced thermogenesis in Mongolian gerbils
title_full Cecal microbial transplantation attenuates hyperthyroid‐induced thermogenesis in Mongolian gerbils
title_fullStr Cecal microbial transplantation attenuates hyperthyroid‐induced thermogenesis in Mongolian gerbils
title_full_unstemmed Cecal microbial transplantation attenuates hyperthyroid‐induced thermogenesis in Mongolian gerbils
title_short Cecal microbial transplantation attenuates hyperthyroid‐induced thermogenesis in Mongolian gerbils
title_sort cecal microbial transplantation attenuates hyperthyroid‐induced thermogenesis in mongolian gerbils
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8913869/
https://www.ncbi.nlm.nih.gov/pubmed/33729663
http://dx.doi.org/10.1111/1751-7915.13793
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