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Reinisch, I.* ; Michenthaler, H.* ; Sulaj, A. ; Moyschewitz, E.* ; Krstic, J.* ; Galhuber, M.* ; Xu, R.* ; Riahi, Z.* ; Wang, T.* ; Vujić, N.* ; Amor, M.* ; Zenezini Chiozzi, R.* ; Wabitsch, M.* ; Kolb, D.* ; Georgiadi, A. ; Glawitsch, L.* ; Heitzer, E.* ; Schulz, T.J.* ; Schupp, M.* ; Sun, W.* ; Dong, H.* ; Ghosh, A.* ; Hoffmann, A. ; Kratky, D.* ; Hinte, L.C.* ; von Meyenn, F.* ; Heck, A.J.R.* ; Blüher, M.* ; Herzig, S. ; Wolfrum, C.* ; Prokesch, A.*

Adipocyte p53 coordinates the response to intermittent fasting by regulating adipose tissue immune cell landscape.

Nat. Commun. 15:1391 (2024)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
In obesity, sustained adipose tissue (AT) inflammation constitutes a cellular memory that limits the effectiveness of weight loss interventions. Yet, the impact of fasting regimens on the regulation of AT immune infiltration is still elusive. Here we show that intermittent fasting (IF) exacerbates the lipid-associated macrophage (LAM) inflammatory phenotype of visceral AT in obese mice. Importantly, this increase in LAM abundance is strongly p53 dependent and partly mediated by p53-driven adipocyte apoptosis. Adipocyte-specific deletion of p53 prevents LAM accumulation during IF, increases the catabolic state of adipocytes, and enhances systemic metabolic flexibility and insulin sensitivity. Finally, in cohorts of obese/diabetic patients, we describe a p53 polymorphism that links to efficacy of a fasting-mimicking diet and that the expression of p53 and TREM2 in AT negatively correlates with maintaining weight loss after bariatric surgery. Overall, our results demonstrate that p53 signalling in adipocytes dictates LAM accumulation in AT under IF and modulates fasting effectiveness in mice and humans.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Acute Kidney Injury; Sex-differences; Atlas; Transcriptomics; Inflammation
Sprache englisch
Veröffentlichungsjahr 2024
HGF-Berichtsjahr 2024
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 15, Heft: 1, Seiten: , Artikelnummer: 1391 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Cancer (IDC)
Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
POF Topic(s) 90000 - German Center for Diabetes Research
30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-501900-251
G-501900-252
G-506501-001
Förderungen EPIC-XS - Horizon 2020 program of the European Union
Deutsches Zentrum fur Diabetesforschung (DZD)
DFG (German Research Foundation)
L-Nutra
German Center for Diabetes Research (DZD)
German Research Foundation (DFG)
City of Graz
Province of Styria
Austrian Science Fund FWF
DOI 10.1038/s41467-024-45724-y
WOS ID 001163439400039
WOS ID 001163439400003
Scopus ID 85185242006
PubMed ID 38360943
Erfassungsdatum 2024-04-22
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