Language
English
Publication Date
4-1-2025
Journal
Nature Metabolism
DOI
10.1038/s42255-025-01268-z
PMID
40211044
PMCID
PMC12509271
PubMedCentral® Posted Date
10-10-2025
PubMedCentral® Full Text Version
Author MSS
Abstract
17β-oestradiol (E2) inhibits overeating and promotes brown adipose tissue (BAT) thermogenesis, whereas prolactin (PRL) does the opposite. During lactation, the simultaneous decline in E2 and surge in PRL contribute to maternal metabolic adaptations, including hyperphagia and suppressed BAT thermogenesis. However, the underlying neuroendocrine mechanisms remain unclear. Here, we find that oestrogen receptor alpha (ERα)-expressing neurons in the medial basal hypothalamus (MBH), specifically the arcuate nucleus of the hypothalamus and the ventrolateral subdivision of the ventromedial hypothalamus (vlVMH), are suppressed during lactation. Deletion of ERα from MBH neurons in virgin female mice induces metabolic phenotypes characteristic of lactation, including hyperprolactinemia, hyperphagia and suppressed BAT thermogenesis. By contrast, activation of ERαvlVMH neurons in lactating mice attenuates these phenotypes. Overall, our study reveals an inhibitory effect of E2–ERαvlVMH signalling on PRL production, which is suppressed during lactation to sustain hyperprolactinemia and metabolic adaptations.
Keywords
Animals, Lactation, Female, Mice, Hyperprolactinemia, Hypothalamus, Prolactin, Estrogens, Signal Transduction, Adaptation, Physiological, Estrogen Receptor alpha, Thermogenesis, Adipose Tissue, Brown, Mice, Inbred C57BL
Published Open-Access
yes
Recommended Citation
Yu, Meng; Feng, Bing; Bean, Jonathan C; et al., "Suppression of Hypothalamic Oestrogenic Signal Sustains Hyperprolactinemia and Metabolic Adaptation in Lactating Mice" (2025). Faculty and Staff Publications. 4848.
https://digitalcommons.library.tmc.edu/baylor_docs/4848
Included in
Health Services Research Commons, Medical Cell Biology Commons, Medical Molecular Biology Commons, Medical Specialties Commons, Microbiology Commons