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<p>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 ERα<sup>vlVMH</sup> neurons in lactating mice attenuates these phenotypes. Overall, our study reveals an inhibitory effect of E2–ERα<sup>vlVMH</sup> signalling on PRL production, which is suppressed during lactation to sustain hyperprolactinemia and metabolic adaptations.</p>

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Suppression of hypothalamic oestrogenic signal sustains hyperprolactinemia and metabolic adaptation in lactating mice

  • 期刊论文

  • 发表日期：

    2025年4月10日

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  • Meng Yu,
  • Bing Feng,
  • Jonathan C. Bean,
  • Qianru Zhao,
  • Yongjie Yang,
  • Hailan Liu,
  • Yongxiang Li,
  • Benjamin P. Eappen,
  • Hesong Liu,
  • Longlong Tu,
  • Kristine M. Conde,
  • Mengjie Wang,
  • Xi Chen,
  • Na Yin,
  • Darah Ave Threat,
  • Nathan Xu,
  • Junying Han,
  • Peiyu Gao,
  • Yi Zhu,
  • Darryl L. Hadsell,
  • Yang He,
  • Pingwen Xu,
  • Yanlin He,
  • Chunmei Wang

摘要

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.