Nature metabolism · 2025
Suppression of hypothalamic oestrogenic signal sustains hyperprolactinemia and metabolic adaptation in lactating mice.
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Yu Meng, Feng Bing, Bean Jonathan C, Zhao Qianru, Yang Yongjie, Liu Hailan, Li Yongxiang, Eappen Benjamin P, Liu Hesong, Tu Longlong, Conde Kristine M, Wang Mengjie, Chen Xi, Yin Na, Threat Darah Ave, Xu Nathan, Han Junying, Gao Peiyu, Zhu Yi, Hadsell Darryl L, He Yang, Xu Pingwen, He Yanlin, Wang Chunmei
Аннотация
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.