Transfer of dysbiotic gut microbiota has beneficial effects on host liver metabolism
Abstract Gut microbiota dysbiosis has been implicated in a variety of systemic disorders, notably metabolic diseases including obesity and impaired liver function, but the underlying mechanisms are uncertain. To investigate this question, we transferred caecal microbiota from either obese or lean mi...
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Springer Nature
2017-03-01
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Series: | Molecular Systems Biology |
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Online Access: | https://doi.org/10.15252/msb.20167356 |
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author | Simon Nicolas Vincent Blasco‐Baque Audren Fournel Jerome Gilleron Pascale Klopp Aurelie Waget Franck Ceppo Alysson Marlin Roshan Padmanabhan Jason S Iacovoni François Tercé Patrice D Cani Jean‐François Tanti Remy Burcelin Claude Knauf Mireille Cormont Matteo Serino |
author_facet | Simon Nicolas Vincent Blasco‐Baque Audren Fournel Jerome Gilleron Pascale Klopp Aurelie Waget Franck Ceppo Alysson Marlin Roshan Padmanabhan Jason S Iacovoni François Tercé Patrice D Cani Jean‐François Tanti Remy Burcelin Claude Knauf Mireille Cormont Matteo Serino |
author_sort | Simon Nicolas |
collection | DOAJ |
description | Abstract Gut microbiota dysbiosis has been implicated in a variety of systemic disorders, notably metabolic diseases including obesity and impaired liver function, but the underlying mechanisms are uncertain. To investigate this question, we transferred caecal microbiota from either obese or lean mice to antibiotic‐free, conventional wild‐type mice. We found that transferring obese‐mouse gut microbiota to mice on normal chow (NC) acutely reduces markers of hepatic gluconeogenesis with decreased hepatic PEPCK activity, compared to non‐inoculated mice, a phenotypic trait blunted in conventional NOD2 KO mice. Furthermore, transferring of obese‐mouse microbiota changes both the gut microbiota and the microbiome of recipient mice. We also found that transferring obese gut microbiota to NC‐fed mice then fed with a high‐fat diet (HFD) acutely impacts hepatic metabolism and prevents HFD‐increased hepatic gluconeogenesis compared to non‐inoculated mice. Moreover, the recipient mice exhibit reduced hepatic PEPCK and G6Pase activity, fed glycaemia and adiposity. Conversely, transfer of lean‐mouse microbiota does not affect markers of hepatic gluconeogenesis. Our findings provide a new perspective on gut microbiota dysbiosis, potentially useful to better understand the aetiology of metabolic diseases. |
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id | doaj-art-b955560a33e845d1b23e5d096d6e2b27 |
institution | Kabale University |
issn | 1744-4292 |
language | English |
publishDate | 2017-03-01 |
publisher | Springer Nature |
record_format | Article |
series | Molecular Systems Biology |
spelling | doaj-art-b955560a33e845d1b23e5d096d6e2b272025-01-12T12:45:37ZengSpringer NatureMolecular Systems Biology1744-42922017-03-0113311710.15252/msb.20167356Transfer of dysbiotic gut microbiota has beneficial effects on host liver metabolismSimon Nicolas0Vincent Blasco‐Baque1Audren Fournel2Jerome Gilleron3Pascale Klopp4Aurelie Waget5Franck Ceppo6Alysson Marlin7Roshan Padmanabhan8Jason S Iacovoni9François Tercé10Patrice D Cani11Jean‐François Tanti12Remy Burcelin13Claude Knauf14Mireille Cormont15Matteo Serino16Institut National de la Santé et de la Recherche Médicale (INSERM)Institut National de la Santé et de la Recherche Médicale (INSERM)Toulouse III, Institut de Recherche en Santé Digestive (IRSD) Team 3, “Intestinal Neuroimmune Interactions” INSERM U1220, Université Paul SabatierINSERM Unité 1065/Centre Méditerranéen de Médecine Moléculaire (C3M), Université Côte d'AzurInstitut National de la Santé et de la Recherche Médicale (INSERM)Institut National de la Santé et de la Recherche Médicale (INSERM)INSERM Unité 1065/Centre Méditerranéen de Médecine Moléculaire (C3M), Université Côte d'AzurToulouse III, Institut de Recherche en Santé Digestive (IRSD) Team 3, “Intestinal Neuroimmune Interactions” INSERM U1220, Université Paul SabatierInstitut National de la Santé et de la Recherche Médicale (INSERM)Institut National de la Santé et de la Recherche Médicale (INSERM)Institut National de la Santé et de la Recherche Médicale (INSERM)Walloon Excellence in Life Sciences and BIOtechnology (WELBIO), Metabolism and Nutrition Research Group, Louvain Drug Research Institute, Université catholique de LouvainINSERM Unité 1065/Centre Méditerranéen de Médecine Moléculaire (C3M), Université Côte d'AzurInstitut National de la Santé et de la Recherche Médicale (INSERM)Toulouse III, Institut de Recherche en Santé Digestive (IRSD) Team 3, “Intestinal Neuroimmune Interactions” INSERM U1220, Université Paul SabatierINSERM Unité 1065/Centre Méditerranéen de Médecine Moléculaire (C3M), Université Côte d'AzurInstitut National de la Santé et de la Recherche Médicale (INSERM)Abstract Gut microbiota dysbiosis has been implicated in a variety of systemic disorders, notably metabolic diseases including obesity and impaired liver function, but the underlying mechanisms are uncertain. To investigate this question, we transferred caecal microbiota from either obese or lean mice to antibiotic‐free, conventional wild‐type mice. We found that transferring obese‐mouse gut microbiota to mice on normal chow (NC) acutely reduces markers of hepatic gluconeogenesis with decreased hepatic PEPCK activity, compared to non‐inoculated mice, a phenotypic trait blunted in conventional NOD2 KO mice. Furthermore, transferring of obese‐mouse microbiota changes both the gut microbiota and the microbiome of recipient mice. We also found that transferring obese gut microbiota to NC‐fed mice then fed with a high‐fat diet (HFD) acutely impacts hepatic metabolism and prevents HFD‐increased hepatic gluconeogenesis compared to non‐inoculated mice. Moreover, the recipient mice exhibit reduced hepatic PEPCK and G6Pase activity, fed glycaemia and adiposity. Conversely, transfer of lean‐mouse microbiota does not affect markers of hepatic gluconeogenesis. Our findings provide a new perspective on gut microbiota dysbiosis, potentially useful to better understand the aetiology of metabolic diseases.https://doi.org/10.15252/msb.20167356gut microbiota transferhepatic glucose productionhigh‐fat dietmetabolic diseasesmicrobiome |
spellingShingle | Simon Nicolas Vincent Blasco‐Baque Audren Fournel Jerome Gilleron Pascale Klopp Aurelie Waget Franck Ceppo Alysson Marlin Roshan Padmanabhan Jason S Iacovoni François Tercé Patrice D Cani Jean‐François Tanti Remy Burcelin Claude Knauf Mireille Cormont Matteo Serino Transfer of dysbiotic gut microbiota has beneficial effects on host liver metabolism Molecular Systems Biology gut microbiota transfer hepatic glucose production high‐fat diet metabolic diseases microbiome |
title | Transfer of dysbiotic gut microbiota has beneficial effects on host liver metabolism |
title_full | Transfer of dysbiotic gut microbiota has beneficial effects on host liver metabolism |
title_fullStr | Transfer of dysbiotic gut microbiota has beneficial effects on host liver metabolism |
title_full_unstemmed | Transfer of dysbiotic gut microbiota has beneficial effects on host liver metabolism |
title_short | Transfer of dysbiotic gut microbiota has beneficial effects on host liver metabolism |
title_sort | transfer of dysbiotic gut microbiota has beneficial effects on host liver metabolism |
topic | gut microbiota transfer hepatic glucose production high‐fat diet metabolic diseases microbiome |
url | https://doi.org/10.15252/msb.20167356 |
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