ArticleNature communications2023
Maternal thyroid hormone receptor β activation in mice sparks brown fat thermogenesis in the offspring.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Triiodothyroacetic acid exerts tissue-specific thyromimetic effects without tachycardia and hyperthermia in male mice.European thyroid journal · 2026Article
- Alternative Receptor Signaling for the Selective and Multifaceted Regulation of Human Brown Adipocytes.International journal of molecular sciences · 2026Review
- Exclusive Breastfeeding Drives AMPK-Dependent Thermogenic Memory in BAT and Promotes Long-Term Metabolic Benefits in Offspring.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Hormones, heat, and health: a comprehensive review of sex-based differences in brown and beige fat biology.Biology of sex differences · 2025Review
- Reduced Availability of Essential Amino Acids Disrupts Differentiation of Anorexigenic POMC Neurons in the Fetal Rat Hypothalamus.Molecular neurobiology · 2025Article
- Sex-specific role of epigenetic modification of a leptin upstream enhancer in adipose tissue.Clinical epigenetics · 2025Article
- Identification of key genes regulating brown adipose tissue thermogenesis in goat kids (Frontiers in veterinary science · 2025Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.