AI Article Synopsis
- Maternal thyroid hormones significantly influence fetal development, but the effects of maternal hyperthyroidism on offspring are not well understood.
- In a mouse study, maternal treatment with the thyroid hormone T3 during pregnancy improved glucose tolerance in male offspring and increased thermogenesis in brown adipose tissue (BAT) in both sexes.
- The study found that proper maternal thyroid hormone receptor β (TRβ) signaling is crucial for these benefits, and alterations in maternal serum metabolites like choline were also observed, linking maternal TRβ activation to specific adaptations in offspring thermoregulation.
Article 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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10597992 | PMC |
| http://dx.doi.org/10.1038/s41467-023-42425-w | DOI Listing |
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