@article{4bb1c202f3be46e8874441f7036fb072,
title = "Systemic GDF11 stimulates the secretion of adiponectin and induces a calorie restriction-like phenotype in aged mice",
abstract = "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.",
keywords = "GDF11, adiponectin, aging, calorie restriction, heterochronic parabiosis, rejuvenation",
author = "Lida Katsimpardi and Nicolas Kuperwasser and Claire Camus and Carine Moigneu and Aur{\'e}lie Chiche and Virginie Tolle and Han Li and Erzsebet Kokovay and Lledo, {Pierre Marie}",
note = "Funding Information: L. K. received a fellowship from LabEx/Revive and a research grant from Inserm “Transversal program on Aging” (AGEMED). A. C. was funded by a postdoctoral fellowship from the Revive Consortium. The Lledo laboratory was supported by national funds (ANR-10-LABX-73, ANR-15-CE37-0004-01, ANR-11-IDEX-0004-02), the life insurance company “AG2R-La-Mondiale” and Laboratoire d'Excellence Revive (Investissement d'Avenir). The Kokovay laboratory acknowledges the Morrison Trust Foundation and the Barshop Institute Nathan Shock Center. The Li laboratory was funded by IP, CNRS and the Agence Nationale de la Recherche (ANR-10-LABX-73, ANR-16-CE13-0017-01), Fondation ARC (PJA 20161205028, 20181208231) and AFM-Telethon Foundation. Funding Information: L. K. received a fellowship from LabEx/Revive and a research grant from Inserm “Transversal program on Aging” (AGEMED). A. C. was funded by a postdoctoral fellowship from the Revive Consortium. The Lledo laboratory was supported by national funds (ANR‐10‐LABX‐73, ANR‐15‐CE37‐0004‐01, ANR‐11‐IDEX‐0004‐02), the life insurance company “AG2R‐La‐Mondiale” and Laboratoire d'Excellence Revive (Investissement d'Avenir). The Kokovay laboratory acknowledges the Morrison Trust Foundation and the Barshop Institute Nathan Shock Center. The Li laboratory was funded by IP, CNRS and the Agence Nationale de la Recherche (ANR‐10‐LABX‐73, ANR‐16‐CE13‐0017‐01), Fondation ARC (PJA 20161205028, 20181208231) and AFM‐Telethon Foundation. Publisher Copyright: {\textcopyright} 2019 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.",
year = "2020",
month = jan,
day = "1",
doi = "10.1111/acel.13038",
language = "English (US)",
volume = "19",
journal = "Aging Cell",
issn = "1474-9718",
publisher = "Wiley-Blackwell",
number = "1",
}