Polyamine metabolism links gut microbiota and testicular dysfunction

Abstract Background Male fertility impaired by exogenous toxins is a serious worldwide issue threatening the health of the new-born and causing infertility. However, the metabolic connection between toxic exposures and testicular dysfunction remains unclear. Results In the present study, the metabol...

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Autores principales: Qi Zhao, Jian-Feng Huang, Yan Cheng, Man-Yun Dai, Wei-Feng Zhu, Xiu-Wei Yang, Frank J. Gonzalez, Fei Li
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Publicado: BMC 2021
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Acceso en línea:https://doaj.org/article/96582235b83142678a6f6dedccf72d38
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spelling oai:doaj.org-article:96582235b83142678a6f6dedccf72d382021-11-14T12:10:18ZPolyamine metabolism links gut microbiota and testicular dysfunction10.1186/s40168-021-01157-z2049-2618https://doaj.org/article/96582235b83142678a6f6dedccf72d382021-11-01T00:00:00Zhttps://doi.org/10.1186/s40168-021-01157-zhttps://doaj.org/toc/2049-2618Abstract Background Male fertility impaired by exogenous toxins is a serious worldwide issue threatening the health of the new-born and causing infertility. However, the metabolic connection between toxic exposures and testicular dysfunction remains unclear. Results In the present study, the metabolic disorder of testicular dysfunction was investigated using triptolide-induced testicular injury in mice. We found that triptolide induced spermine deficiency resulting from disruption of polyamine biosynthesis and uptake in testis, and perturbation of the gut microbiota. Supplementation with exogenous spermine reversed triptolide-induced testicular dysfunction through increasing the expression of genes related to early and late spermatogenic events, as well as increasing the reduced number of offspring. Loss of gut microbiota by antibiotic treatment resulted in depletion of spermine levels in the intestine and potentiation of testicular injury. Testicular dysfunction in triptolide-treated mice was reversed by gut microbial transplantation from untreated mice and supplementation with polyamine-producing Parabacteroides distasonis. The protective effect of spermine during testicular injury was largely dependent on upregulation of heat shock protein 70s (HSP70s) both in vivo and in vitro. Conclusions The present study linked alterations in the gut microbiota to testicular dysfunction through disruption of polyamine metabolism. The diversity and dynamics of the gut microbiota may be considered as a therapeutic option to prevent male infertility. Video AbstractQi ZhaoJian-Feng HuangYan ChengMan-Yun DaiWei-Feng ZhuXiu-Wei YangFrank J. GonzalezFei LiBMCarticleTesticular dysfunctionGut microbiotaPolyamine metabolismMetabolomicsMicrobial ecologyQR100-130ENMicrobiome, Vol 9, Iss 1, Pp 1-18 (2021)
institution DOAJ
collection DOAJ
language EN
topic Testicular dysfunction
Gut microbiota
Polyamine metabolism
Metabolomics
Microbial ecology
QR100-130
spellingShingle Testicular dysfunction
Gut microbiota
Polyamine metabolism
Metabolomics
Microbial ecology
QR100-130
Qi Zhao
Jian-Feng Huang
Yan Cheng
Man-Yun Dai
Wei-Feng Zhu
Xiu-Wei Yang
Frank J. Gonzalez
Fei Li
Polyamine metabolism links gut microbiota and testicular dysfunction
description Abstract Background Male fertility impaired by exogenous toxins is a serious worldwide issue threatening the health of the new-born and causing infertility. However, the metabolic connection between toxic exposures and testicular dysfunction remains unclear. Results In the present study, the metabolic disorder of testicular dysfunction was investigated using triptolide-induced testicular injury in mice. We found that triptolide induced spermine deficiency resulting from disruption of polyamine biosynthesis and uptake in testis, and perturbation of the gut microbiota. Supplementation with exogenous spermine reversed triptolide-induced testicular dysfunction through increasing the expression of genes related to early and late spermatogenic events, as well as increasing the reduced number of offspring. Loss of gut microbiota by antibiotic treatment resulted in depletion of spermine levels in the intestine and potentiation of testicular injury. Testicular dysfunction in triptolide-treated mice was reversed by gut microbial transplantation from untreated mice and supplementation with polyamine-producing Parabacteroides distasonis. The protective effect of spermine during testicular injury was largely dependent on upregulation of heat shock protein 70s (HSP70s) both in vivo and in vitro. Conclusions The present study linked alterations in the gut microbiota to testicular dysfunction through disruption of polyamine metabolism. The diversity and dynamics of the gut microbiota may be considered as a therapeutic option to prevent male infertility. Video Abstract
format article
author Qi Zhao
Jian-Feng Huang
Yan Cheng
Man-Yun Dai
Wei-Feng Zhu
Xiu-Wei Yang
Frank J. Gonzalez
Fei Li
author_facet Qi Zhao
Jian-Feng Huang
Yan Cheng
Man-Yun Dai
Wei-Feng Zhu
Xiu-Wei Yang
Frank J. Gonzalez
Fei Li
author_sort Qi Zhao
title Polyamine metabolism links gut microbiota and testicular dysfunction
title_short Polyamine metabolism links gut microbiota and testicular dysfunction
title_full Polyamine metabolism links gut microbiota and testicular dysfunction
title_fullStr Polyamine metabolism links gut microbiota and testicular dysfunction
title_full_unstemmed Polyamine metabolism links gut microbiota and testicular dysfunction
title_sort polyamine metabolism links gut microbiota and testicular dysfunction
publisher BMC
publishDate 2021
url https://doaj.org/article/96582235b83142678a6f6dedccf72d38
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AT jianfenghuang polyaminemetabolismlinksgutmicrobiotaandtesticulardysfunction
AT yancheng polyaminemetabolismlinksgutmicrobiotaandtesticulardysfunction
AT manyundai polyaminemetabolismlinksgutmicrobiotaandtesticulardysfunction
AT weifengzhu polyaminemetabolismlinksgutmicrobiotaandtesticulardysfunction
AT xiuweiyang polyaminemetabolismlinksgutmicrobiotaandtesticulardysfunction
AT frankjgonzalez polyaminemetabolismlinksgutmicrobiotaandtesticulardysfunction
AT feili polyaminemetabolismlinksgutmicrobiotaandtesticulardysfunction
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