Clues to quality of journals
Open Access Policy of Helmholtz Association 2016
CC Licencences
Publication Metrics
Home
Deutsch
New EVA Application
Advanced Search
Browse by ...
Publication overview
Statistics (last 5 years)
OA Publications
Submit Publication
Import publication from...
Report missing publication
Contact persons
Help
Text
Endnote (RIS)
BibTeX
Publ. Version/Full Text
DOI
PMC
 |
Open Access Gold |
|
as soon as is submitted to ZB.
Maternal thyroid hormone receptor β activation in mice sparks brown fat thermogenesis in the offspring.
Nat. Commun. 14:6742 (2023)
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.
Impact Factor
Scopus SNIP
Altmetric
16.600
0.000
Annotations
Special Publikation
Hide on homepage
Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Adipose-tissue; Subclinical Hypothyroidism; Brain-development; Hypothyroxinemia; Pregnancy; Fetal; Resistance; Still; Ucp1; Bat
Language
english
Publication Year
2023
HGF-reported in Year
2023
ISSN (print) / ISBN
2041-1723
e-ISSN
2041-1723
Journal
Nature Communications
Quellenangaben
Volume: 14,
Issue: 1,
Article Number: 6742
Publisher
Nature Publishing Group
Publishing Place
London
Reviewing status
Peer reviewed
Institute(s)
Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
POF-Topic(s)
30201 - Metabolic Health
Research field(s)
Helmholtz Diabetes Center
PSP Element(s)
G-506501-001
Grants
Projekt DEAL.
Medical Faculty of the University of Lubeck
Deutsche Forschungsgemeinschaft
Medical Faculty of the University of Lubeck
Deutsche Forschungsgemeinschaft
WOS ID
001089230100017
Scopus ID
85174567134
PubMed ID
37875497
Erfassungsdatum
2023-11-28