Open AccessSystemic GDF11 stimulates the secretion of adiponectin and induces a calorie restriction‐like phenotype in aged mice
Author(s) -
Katsimpardi Lida,
Kuperwasser Nicolas,
Camus Claire,
Moigneu Carine,
Chiche Aurélie,
Tolle Virginie,
Li Han,
Kokovay Erzsebet,
Lledo PierreMarie
Publication year - 2020
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/acel.13038
Subject(s) - biology , calorie restriction , parabiosis , endocrinology , adiponectin , medicine , energy homeostasis , adipose tissue , regulator , phenotype , neurogenesis , adipogenesis , appetite , white adipose tissue , fgf21 , insulin , microbiology and biotechnology , obesity , fibroblast growth factor , insulin resistance , genetics , gene , receptor
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.