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<p>Heat stress triggers defensive energy demands to prevent cellular damage. Using male mice, we found that exposure to high ambient temperature (HAT) induces an increase in intestinal glucose absorption mediated by sodium/glucose cotransporter 1 (SGLT1). Glucose supplementation alleviated HAT-induced physiological damage in mice. Mechanistically, we found that blocking intestinal vagal motor nerve transmission eliminated HAT’s stimulatory effects on intestinal glucose absorption. This suggests that cholinergic motor neurons originating from the dorsal motor nucleus of the vagus (DMV<sup>ChAT</sup>) play a crucial role. Transneuronal tracing revealed an ascending pathway from glutamatergic neurons in the medial preoptic area (mPOA<sup>Glu</sup>) to the vagus nerve, with corticotropin-releasing factor neurons in the paraventricular nucleus of the hypothalamus (PVN<sup>CRF</sup>) acting as a key relay. Inhibiting key neurons in the mPOA<sup>Glu</sup> → PVN<sup>CRF</sup> → DMV<sup>ChAT</sup> circuit mimicked the effects of vagus blockage on HAT-induced intestinal glucose absorption. Our findings establish the brain-vagal-gut pathway as an interoceptive circuit for adapting to HAT challenges.</p>

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High ambient temperature activates a neural circuit for gut glucose uptake in male mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月14日

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  • Ruihua Li,
  • Mingming Liu,
  • Zhiqi Zhang,
  • Qin Zhu,
  • Mingsi Chen,
  • Jiaxin Liu,
  • Linghui Pan,
  • Aru Su,
  • Qian Zhou,
  • Renli Qi,
  • Zuohua Liu,
  • Ruifan Wu,
  • Songbo Wang,
  • Lina Wang,
  • Gang Shu,
  • Pingwen Xu,
  • Qingyan Jiang,
  • Canjun Zhu

摘要

Heat stress triggers defensive energy demands to prevent cellular damage. Using male mice, we found that exposure to high ambient temperature (HAT) induces an increase in intestinal glucose absorption mediated by sodium/glucose cotransporter 1 (SGLT1). Glucose supplementation alleviated HAT-induced physiological damage in mice. Mechanistically, we found that blocking intestinal vagal motor nerve transmission eliminated HAT’s stimulatory effects on intestinal glucose absorption. This suggests that cholinergic motor neurons originating from the dorsal motor nucleus of the vagus (DMVChAT) play a crucial role. Transneuronal tracing revealed an ascending pathway from glutamatergic neurons in the medial preoptic area (mPOAGlu) to the vagus nerve, with corticotropin-releasing factor neurons in the paraventricular nucleus of the hypothalamus (PVNCRF) acting as a key relay. Inhibiting key neurons in the mPOAGlu → PVNCRF → DMVChAT circuit mimicked the effects of vagus blockage on HAT-induced intestinal glucose absorption. Our findings establish the brain-vagal-gut pathway as an interoceptive circuit for adapting to HAT challenges.