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Oelkrug, R.* ; Harder, L.* ; Pedaran, M.* ; Hoffmann, A. ; Kolms, B.* ; Inderhees, J.* ; Gachkar, S.* ; Resch, J.* ; Johann, K.* ; Jöhren, O.* ; Krause, K.* ; Mittag, J.*

Maternal thyroid hormone receptor β activation in mice sparks brown fat thermogenesis in the offspring.

Nat. Commun. 14:6742 (2023)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
It is well established that maternal thyroid hormones play an important role for the developing fetus; however, the consequences of maternal hyperthyroidism for the offspring remain poorly understood. Here we show in mice that maternal 3,3',5-triiodothyronine (T3) treatment during pregnancy leads to improved glucose tolerance in the adult male offspring and hyperactivity of brown adipose tissue (BAT) thermogenesis in both sexes starting early after birth. The activated BAT provides advantages upon cold exposure, reducing the strain on other thermogenic organs like muscle. This maternal BAT programming requires intact maternal thyroid hormone receptor β (TRβ) signaling, as offspring of mothers lacking this receptor display the opposite phenotype. On the molecular level, we identify distinct T3 induced alterations in maternal serum metabolites, including choline, a key metabolite for healthy pregnancy. Taken together, our results connect maternal TRβ activation to the fetal programming of a thermoregulatory phenotype in the offspring.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Adipose-tissue; Subclinical Hypothyroidism; Brain-development; Hypothyroxinemia; Pregnancy; Fetal; Resistance; Still; Ucp1; Bat
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 14, Heft: 1, Seiten: , Artikelnummer: 6742 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
Förderungen Projekt DEAL.
Medical Faculty of the University of Lubeck
Deutsche Forschungsgemeinschaft