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

Rebecca Oelkrug, Lisbeth Harder, Mehdi Pedaran, Anne Hoffmann, Beke Kolms, Julica Inderhees, Sogol Gachkar, Julia Resch, Kornelia Johann, Olaf Jöhren, Kerstin Krause, Jens Mittag*

*Corresponding author for this work


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.

Original languageEnglish
Article number6742
JournalNature Communications
Issue number1
Pages (from-to)6742
Publication statusPublished - 12.2023

Research Areas and Centers

  • Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)

DFG Research Classification Scheme

  • 205-17 Endocrinology, Diabetology, Metabolism

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