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Roth, L.* ; Hoffmann, A. ; Hagemann, T. ; Wagner, L.* ; Strehlau, C. ; Sheikh, B. ; Donndorf, L. ; Ghosh, A.* ; Noé, F.* ; Wolfrum, C.* ; Krohn, K.* ; Weiner, J.* ; Heiker, J.T. ; Klöting, N. ; Stumvoll, M. ; Tönjes, A.* ; Blüher, M. ; Mittag, J.* ; Krause, K.*

Thyroid hormones are required for thermogenesis of beige adipocytes induced by Zfp423 inactivation.

Cell Rep. 43:114987 (2024)
Verlagsversion DOI PMC
Free journal
Creative Commons Lizenzvertrag
The significance of thyroid hormones (THs) in beige adipocyte thermogenesis remains incompletely understood. We previously reported that THs directly regulate the expression of zinc-finger protein 423 (ZFP423), an anti-thermogenic factor, in adipose tissue. This study investigates the interaction between THs and adrenergic signaling in regulating thermogenic capacity and activation of beige adipocytes formed in response to Zfp423 deletion. We demonstrate that THs are indispensable for uncoupling protein 1 (UCP1)-dependent thermogenesis, leading to increased energy expenditure in mice with adipocyte-specific Zfp423 knockout. Targeted activation of the thyroid receptor isoform TRβ, which plays a central role in the inguinal depot, is sufficient to enhance energy expenditure in hypothyroid Zfp423iAKO mice. Mechanistically, THs and ZFP423 pathways cooperate to regulate early B cell factor 2 (EBF2)-mediated activation of the Ucp1 gene. RNA sequencing (RNA-seq) analysis of human adipose tissue samples supports the relevance of this regulatory network for human adipose tissue plasticity.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Cp: Metabolism ; Cp: Molecular Biology ; Ebf2 ; Ucp1 ; Zfp423 ; Adrenergic Signaling ; Beige Adipocytes ; Browning ; Norepinephrine ; Thermogenesis ; Thyroid Hormone Receptor Beta ; Thyroid Hormones; Brown Adipose-tissue; Transcriptional Control; White; Receptor; Triiodothyronine; Glucose; Activation; Conversion; Thyroxine; Obesity
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Zeitschrift Cell Reports
Quellenangaben Band: 43, Heft: 12, Seiten: , Artikelnummer: 114987 Supplement: ,
Verlag Cell Press
Verlagsort 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
Förderungen German Federal Ministry of Education and Research (BMBF) through the German Center for Diabetes Research (DZD e.V.)
Ministry of Culture and Science of the state of North Rhine-Westphalia (Dusseldorf, Germany)
German Federal Ministry of Health (Berlin, Germany)
Helmholtz Munich
Free State of Saxony
German Research Foundation (DFG)