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Wueest, S.* ; Scaffidi, C.* ; van Krieken, P.P.* ; Konrad, N.K.* ; Koch, C.* ; Lempesis, I.G.* ; Fullin, J.* ; Manolopoulos, K.N.* ; Böttcher, S.* ; Goossens, G.H.* ; Blüher, M. ; Konrad, D.*

Expression of p53 in human adipose tissue correlates positively with FAS and BMI.

Int. J. Obes., DOI: 10.1038/s41366-024-01691-4 (2024)
Verlagsversion DOI PMC
Open Access Hybrid
Creative Commons Lizenzvertrag
Activation of Fas (CD95) in adipocytes inhibits browning and may contribute to body weight gain in mice. Moreover, Fas expression in white adipose tissue (WAT) correlates positively with body mass index (BMI) in humans. However, molecular pathways involved in the inhibitory effect of Fas on energy metabolism remain incompletely understood. Herein, we report that protein levels of the tumor suppressor p53 were reduced in primary white adipocytes of adipocyte-specific Fas-knockout mice. Moreover, Fas ligand (FasL) treatment increased p53 concentrations in cultured adipocytes and decreased mitochondrial oxygen consumption in control but not in p53-depleted cells, indicating that Fas activation reduces energy expenditure in a p53-dependent manner. In line, in differentiated human mesenchymal stem cells and WAT derived from different anatomical depots, FAS expression was positively associated with p53. Furthermore, p53 expression in human subcutaneous and visceral WAT correlated positively with BMI, whereas its expression in visceral WAT was inversely associated with insulin sensitivity (as assessed by hyperinsulinemic-euglycemic clamp). Taken together, our data suggest that Fas regulates p53 expression in adipocytes, and may thereby affect body weight gain and insulin sensitivity.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Insulin-resistance; Inflammation
Sprache englisch
Veröffentlichungsjahr 2024
HGF-Berichtsjahr 2024
ISSN (print) / ISBN 0307-0565
e-ISSN 1476-5497
Zeitschrift International Journal of Obesity
Verlag Nature Publishing Group
Verlagsort Campus, 4 Crinan St, London, N1 9xw, England
Begutachtungsstatus Peer reviewed
Institut(e) Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
POF Topic(s) 30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-506501-001
Förderungen University of Zurich
University of Birmingham (UK)
Maastricht University (the Netherlands)
European Foundation
Deutsche Forschungsgemeinschaft (DFG, German Research Foundation)
Swiss National Science Foundation
DOI 10.1038/s41366-024-01691-4
WOS ID 001367349700001
Scopus ID 85211181329
PubMed ID 39617842
Erfassungsdatum 2024-12-06
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