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 and Jens Mittag ()
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Rebecca Oelkrug: University of Lübeck
Lisbeth Harder: University of Lübeck
Mehdi Pedaran: University of Lübeck
Anne Hoffmann: Helmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG) of the Helmholtz Zentrum München at the University of Leipzig and University Hospital Leipzig
Beke Kolms: University of Lübeck
Julica Inderhees: University of Lübeck
Sogol Gachkar: University of Lübeck
Julia Resch: University of Lübeck
Kornelia Johann: University of Lübeck
Olaf Jöhren: University of Lübeck
Kerstin Krause: University of Leipzig Medical Center
Jens Mittag: University of Lübeck

Nature Communications, 2023, vol. 14, issue 1, 1-14

Abstract: Abstract 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.

Date: 2023
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DOI: 10.1038/s41467-023-42425-w

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