GDF15 Provides an Endocrine Signal of Nutritional Stress in Mice and Humans.
GDF15
GFRAL
conditioned taste aversion
integrated stress response
overnutrion
Journal
Cell metabolism
ISSN: 1932-7420
Titre abrégé: Cell Metab
Pays: United States
ID NLM: 101233170
Informations de publication
Date de publication:
05 03 2019
05 03 2019
Historique:
received:
20
07
2018
revised:
10
10
2018
accepted:
17
12
2018
pubmed:
15
1
2019
medline:
12
5
2020
entrez:
15
1
2019
Statut:
ppublish
Résumé
GDF15 is an established biomarker of cellular stress. The fact that it signals via a specific hindbrain receptor, GFRAL, and that mice lacking GDF15 manifest diet-induced obesity suggest that GDF15 may play a physiological role in energy balance. We performed experiments in humans, mice, and cells to determine if and how nutritional perturbations modify GDF15 expression. Circulating GDF15 levels manifest very modest changes in response to moderate caloric surpluses or deficits in mice or humans, differentiating it from classical intestinally derived satiety hormones and leptin. However, GDF15 levels do increase following sustained high-fat feeding or dietary amino acid imbalance in mice. We demonstrate that GDF15 expression is regulated by the integrated stress response and is induced in selected tissues in mice in these settings. Finally, we show that pharmacological GDF15 administration to mice can trigger conditioned taste aversion, suggesting that GDF15 may induce an aversive response to nutritional stress.
Identifiants
pubmed: 30639358
pii: S1550-4131(18)30753-8
doi: 10.1016/j.cmet.2018.12.016
pmc: PMC6408327
pii:
doi:
Substances chimiques
GDF15 protein, human
0
Gdf15 protein, mouse
0
Growth Differentiation Factor 15
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
707-718.e8Subventions
Organisme : Wellcome Trust
ID : 200848/Z/16/Z
Pays : United Kingdom
Organisme : Department of Health
Pays : United Kingdom
Organisme : NIGMS NIH HHS
ID : U54 GM104940
Pays : United States
Organisme : Wellcome Trust
ID : 106263/Z/14/Z
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 095515/Z/11/Z
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_00014/5
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_12012/1
Pays : United Kingdom
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Medical Research Council
ID : G0600717
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_00014/2
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_12012/3
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_00014/3
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 107064
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_12012/2
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 106262/Z/14/Z
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 098497/Z/12/Z
Pays : United Kingdom
Organisme : Medical Research Council
ID : G0802051
Pays : United Kingdom
Organisme : Medical Research Council
ID : G9824984
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 100574/Z/12/Z
Pays : United Kingdom
Organisme : Medical Research Council
ID : G0900554
Pays : United Kingdom
Organisme : Medical Research Council
ID : G0400192
Pays : United Kingdom
Organisme : Wellcome Trust
ID : WT 107064
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_00014/1
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 100140
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UU_12012/5
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RG/12/13/29853
Pays : United Kingdom
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.
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