Systemic GDF11 stimulates the secretion of adiponectin and induces a calorie restriction-like phenotype in aged mice.


Journal

Aging cell
ISSN: 1474-9726
Titre abrégé: Aging Cell
Pays: England
ID NLM: 101130839

Informations de publication

Date de publication:
01 2020
Historique:
received: 28 01 2019
revised: 06 07 2019
accepted: 19 08 2019
pubmed: 23 10 2019
medline: 14 1 2021
entrez: 23 10 2019
Statut: ppublish

Résumé

Aging is a negative regulator of general homeostasis, tissue function, and regeneration. Changes in organismal energy levels and physiology, through systemic manipulations such as calorie restriction and young blood infusion, can regenerate tissue activity and increase lifespan in aged mice. However, whether these two systemic manipulations could be linked has never been investigated. Here, we report that systemic GDF11 triggers a calorie restriction-like phenotype without affecting appetite or GDF15 levels in the blood, restores the insulin/IGF-1 signaling pathway, and stimulates adiponectin secretion from white adipose tissue by direct action on adipocytes, while repairing neurogenesis in the aged brain. These findings suggest that GDF11 has a pleiotropic effect on an organismal level and that it could be a linking mechanism of rejuvenation between heterochronic parabiosis and calorie restriction. As such, GDF11 could be considered as an important therapeutic candidate for age-related neurodegenerative and metabolic disorders.

Identifiants

pubmed: 31637864
doi: 10.1111/acel.13038
pmc: PMC6974718
doi:

Substances chimiques

Adiponectin 0
Bone Morphogenetic Proteins 0
Gdf11 protein, mouse 0
Growth Differentiation Factors 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e13038

Subventions

Organisme : Agence Nationale de Recherche
ID : ANR-10-LABX-73
Pays : International
Organisme : Agence Nationale de Recherche
ID : ANR-11-IDEX-0004-02
Pays : International
Organisme : Agence Nationale de Recherche
ID : ANR-15-CE37-0004-01
Pays : International
Organisme : Morrison Trust Foundation
Pays : International
Organisme : Barshop Institute Nathan Shock Center
Pays : International

Informations de copyright

© 2019 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.

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Auteurs

Lida Katsimpardi (L)

Perception and Memory Lab, Neuroscience Department, Institut Pasteur, Paris, France.
Centre National de la Recherche Scientifique, Unité Mixte de Recherche 3571, Paris, France.

Nicolas Kuperwasser (N)

Department of Cell Growth and Signaling, Institut National de la Santé et de la Recherche Médicale (INSERM) U1151, Institut Necker Enfants Malades (INEM), Université Paris Descartes, France.

Claire Camus (C)

Perception and Memory Lab, Neuroscience Department, Institut Pasteur, Paris, France.
Centre National de la Recherche Scientifique, Unité Mixte de Recherche 3571, Paris, France.

Carine Moigneu (C)

Perception and Memory Lab, Neuroscience Department, Institut Pasteur, Paris, France.
Centre National de la Recherche Scientifique, Unité Mixte de Recherche 3571, Paris, France.

Aurélie Chiche (A)

Department of Developmental & Stem Cell Biology, Cellular Plasticity & Disease Modelling, CNRS UMR 3738, Institut Pasteur, Paris, France.

Virginie Tolle (V)

Centre de Psychiatrie et Neurosciences, UMR-S 894, INSERM, Université Paris Descartes Sorbonne Paris Cité, Paris, France.

Han Li (H)

Department of Developmental & Stem Cell Biology, Cellular Plasticity & Disease Modelling, CNRS UMR 3738, Institut Pasteur, Paris, France.

Erzsebet Kokovay (E)

Cell Systems and Anatomy, Brashop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.

Pierre-Marie Lledo (PM)

Perception and Memory Lab, Neuroscience Department, Institut Pasteur, Paris, France.
Centre National de la Recherche Scientifique, Unité Mixte de Recherche 3571, Paris, France.

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