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Klein, A.B.* ; Nicolaisen, T.S.* ; Ørtenblad, N.* ; Gejl, K.D.* ; Jensen, R.* ; Fritzen, A.M.* ; Larsen, E.L.* ; Karstoft, K.* ; Poulsen, H.E.* ; Morville, T.* ; Sahl, R.E.* ; Helge, J.W.* ; Lund, J.* ; Falk, S.* ; Lyngbæk, M.* ; Ellingsgaard, H.* ; Pedersen, B.K.* ; Lu, W.* ; Finan, B.* ; Jørgensen, S.B.* ; Seeley, R.J.* ; Kleinert, M. ; Kiens, B.* ; Richter, E.A.* ; Clemmensen, C.*

Pharmacological but not physiological GDF15 suppresses feeding and the motivation to exercise.

Nat. Commun. 12:1041 (2021)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Growing evidence supports that pharmacological application of growth differentiation factor 15 (GDF15) suppresses appetite but also promotes sickness-like behaviors in rodents via GDNF family receptor α-like (GFRAL)-dependent mechanisms. Conversely, the endogenous regulation of GDF15 and its physiological effects on energy homeostasis and behavior remain elusive. Here we show, in four independent human studies that prolonged endurance exercise increases circulating GDF15 to levels otherwise only observed in pathophysiological conditions. This exercise-induced increase can be recapitulated in mice and is accompanied by increased Gdf15 expression in the liver, skeletal muscle, and heart muscle. However, whereas pharmacological GDF15 inhibits appetite and suppresses voluntary running activity via GFRAL, the physiological induction of GDF15 by exercise does not. In summary, exercise-induced circulating GDF15 correlates with the duration of endurance exercise. Yet, higher GDF15 levels after exercise are not sufficient to evoke canonical pharmacological GDF15 effects on appetite or responsible for diminishing exercise motivation.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Muscle Glycogen; Receptor; Increases; Biomarker; Level
Sprache englisch
Veröffentlichungsjahr 2021
HGF-Berichtsjahr 2021
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 12, Heft: 1, Seiten: , Artikelnummer: 1041 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)
POF Topic(s) 30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502200-001
Förderungen NIDDK NIH HHS
DOI 10.1038/s41467-021-21309-x
WOS ID WOS:000626747000021
PubMed ID 33589633
Erfassungsdatum 2021-05-11
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