Corrupted adipose tissue endogenous myelopoiesis initiates diet-induced metabolic disease

Activation and increased numbers of inflammatory macrophages, in adipose tissue (AT) are deleterious in metabolic diseases. Up to now, AT macrophages (ATM) accumulation was considered to be due to blood infiltration or local proliferation, although the presence of resident hematopoietic stem/progeni...

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Main Authors: Elodie Luche, Virginie Robert, Vincent Cuminetti, Celine Pomié, Quentin Sastourné-Arrey, Aurélie Waget, Emmanuelle Arnaud, Audrey Varin, Elodie Labit, Patrick Laharrague, Remy Burcelin, Louis Casteilla, Beatrice Cousin
Format: Article
Language:English
Published: eLife Sciences Publications Ltd 2017-06-01
Series:eLife
Subjects:
Online Access:https://elifesciences.org/articles/23194
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author Elodie Luche
Virginie Robert
Vincent Cuminetti
Celine Pomié
Quentin Sastourné-Arrey
Aurélie Waget
Emmanuelle Arnaud
Audrey Varin
Elodie Labit
Patrick Laharrague
Remy Burcelin
Louis Casteilla
Beatrice Cousin
author_facet Elodie Luche
Virginie Robert
Vincent Cuminetti
Celine Pomié
Quentin Sastourné-Arrey
Aurélie Waget
Emmanuelle Arnaud
Audrey Varin
Elodie Labit
Patrick Laharrague
Remy Burcelin
Louis Casteilla
Beatrice Cousin
author_sort Elodie Luche
collection DOAJ
description Activation and increased numbers of inflammatory macrophages, in adipose tissue (AT) are deleterious in metabolic diseases. Up to now, AT macrophages (ATM) accumulation was considered to be due to blood infiltration or local proliferation, although the presence of resident hematopoietic stem/progenitor cells (Lin-/Sca+/c-Kit+; LSK phenotype) in the AT (AT-LSK) has been reported. By using transplantation of sorted AT-LSK and gain and loss of function studies we show that some of the inflammatory ATM inducing metabolic disease, originate from resident AT-LSK. Transplantation of AT-LSK sorted from high fat diet-fed (HFD) mice is sufficient to induce ATM accumulation, and to transfer metabolic disease in control mice. Conversely, the transplantation of control AT-LSK improves both AT-inflammation and glucose homeostasis in HFD mice. Our results clearly demonstrate that resident AT-LSK are one of the key point of metabolic disease, and could thus constitute a new promising therapeutic target to fight against metabolic disease.
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spelling doaj.art-a36efdf50ddf4a528c94d1e075a614942022-12-22T04:32:24ZengeLife Sciences Publications LtdeLife2050-084X2017-06-01610.7554/eLife.23194Corrupted adipose tissue endogenous myelopoiesis initiates diet-induced metabolic diseaseElodie Luche0Virginie Robert1Vincent Cuminetti2Celine Pomié3Quentin Sastourné-Arrey4Aurélie Waget5Emmanuelle Arnaud6Audrey Varin7Elodie Labit8Patrick Laharrague9Remy Burcelin10Louis Casteilla11Beatrice Cousin12https://orcid.org/0000-0003-2952-4601STROMALab, Université de Toulouse, CNRS ERL 5311, EFS, INP-ENVT, Inserm U1031, UPS, Toulouse, FranceSTROMALab, Université de Toulouse, CNRS ERL 5311, EFS, INP-ENVT, Inserm U1031, UPS, Toulouse, FranceSTROMALab, Université de Toulouse, CNRS ERL 5311, EFS, INP-ENVT, Inserm U1031, UPS, Toulouse, FranceINSERM U1048, Université de Toulouse, EFS, INP-ENVT, Inserm U1031, UPS, Toulouse, FranceSTROMALab, Université de Toulouse, CNRS ERL 5311, EFS, INP-ENVT, Inserm U1031, UPS, Toulouse, FranceINSERM U1048, Université de Toulouse, EFS, INP-ENVT, Inserm U1031, UPS, Toulouse, FranceSTROMALab, Université de Toulouse, CNRS ERL 5311, EFS, INP-ENVT, Inserm U1031, UPS, Toulouse, FranceSTROMALab, Université de Toulouse, EFS, INP-ENVT, Inserm U1031, UPS, Toulouse, FranceSTROMALab, Université de Toulouse, CNRS ERL 5311, EFS, INP-ENVT, Inserm U1031, UPS, Toulouse, FranceSTROMALab, Université de Toulouse, CNRS ERL 5311, EFS, INP-ENVT, Inserm U1031, UPS, Toulouse, FranceINSERM U1048, Université de Toulouse, EFS, INP-ENVT, Inserm U1031, UPS, Toulouse, FranceSTROMALab, Université de Toulouse, CNRS ERL 5311, EFS, INP-ENVT, Inserm U1031, UPS, Toulouse, FranceSTROMALab, Université de Toulouse, CNRS ERL 5311, EFS, INP-ENVT, Inserm U1031, UPS, Toulouse, FranceActivation and increased numbers of inflammatory macrophages, in adipose tissue (AT) are deleterious in metabolic diseases. Up to now, AT macrophages (ATM) accumulation was considered to be due to blood infiltration or local proliferation, although the presence of resident hematopoietic stem/progenitor cells (Lin-/Sca+/c-Kit+; LSK phenotype) in the AT (AT-LSK) has been reported. By using transplantation of sorted AT-LSK and gain and loss of function studies we show that some of the inflammatory ATM inducing metabolic disease, originate from resident AT-LSK. Transplantation of AT-LSK sorted from high fat diet-fed (HFD) mice is sufficient to induce ATM accumulation, and to transfer metabolic disease in control mice. Conversely, the transplantation of control AT-LSK improves both AT-inflammation and glucose homeostasis in HFD mice. Our results clearly demonstrate that resident AT-LSK are one of the key point of metabolic disease, and could thus constitute a new promising therapeutic target to fight against metabolic disease.https://elifesciences.org/articles/23194adipose tissuediabetesmacrophageshematopoiesis
spellingShingle Elodie Luche
Virginie Robert
Vincent Cuminetti
Celine Pomié
Quentin Sastourné-Arrey
Aurélie Waget
Emmanuelle Arnaud
Audrey Varin
Elodie Labit
Patrick Laharrague
Remy Burcelin
Louis Casteilla
Beatrice Cousin
Corrupted adipose tissue endogenous myelopoiesis initiates diet-induced metabolic disease
eLife
adipose tissue
diabetes
macrophages
hematopoiesis
title Corrupted adipose tissue endogenous myelopoiesis initiates diet-induced metabolic disease
title_full Corrupted adipose tissue endogenous myelopoiesis initiates diet-induced metabolic disease
title_fullStr Corrupted adipose tissue endogenous myelopoiesis initiates diet-induced metabolic disease
title_full_unstemmed Corrupted adipose tissue endogenous myelopoiesis initiates diet-induced metabolic disease
title_short Corrupted adipose tissue endogenous myelopoiesis initiates diet-induced metabolic disease
title_sort corrupted adipose tissue endogenous myelopoiesis initiates diet induced metabolic disease
topic adipose tissue
diabetes
macrophages
hematopoiesis
url https://elifesciences.org/articles/23194
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