Researchers have advocated elevating mouse housing temperatures from the conventional ~22 °C to the mouse thermoneutral point of 30 °C to enhance translational research. However, the impact of environmental temperature on mouse gastrointestinal physiology remains largely unexplored. Here we show that mice raised at 22 °C exhibit whole gut transit speed nearly twice as fast as those raised at 30 °C, primarily driven by a threefold increase in colon transit speed. Furthermore, gut microbiota composition differs between the two temperatures but does not dictate temperature-dependent differences in gut motility. Notably, increased stress signals from the hypothalamic–pituitary–adrenal axis at 22 °C have a pivotal role in mediating temperature-dependent differences in gut motility. Pharmacological and genetic depletion of the stress hormone corticotropin-releasing hormone slows gut motility in stressed 22 °C mice but has no comparable effect in relatively unstressed 30 °C mice. In conclusion, our findings highlight that colder mouse facility temperatures significantly increase gut motility through hormonal stress pathways.

研究人员主张将小鼠外壳温度从传统的约 22 °C 提高到小鼠热中性点 30 °C，以加强转化研究。然而，环境温度对小鼠胃肠道生理学的影响在很大程度上仍未被探索。在这里，我们发现在 22°C 下饲养的小鼠的整个肠道转运速度几乎是在 30°C 下饲养的小鼠的两倍，这主要是由于结肠转运速度增加了三倍。此外，肠道微生物群组成在两种温度之间有所不同，但并不决定肠道运动的温度依赖性差异。值得注意的是，22°C 时下丘脑-垂体-肾上腺轴的应激信号增加在调节肠道运动的温度依赖性差异方面发挥着关键作用。应激激素促肾上腺皮质激素释放激素的药理和遗传耗竭会减慢22°C应激小鼠的肠道蠕动，但对相对无应激的30°C小鼠没有类似的影响。总之，我们的研究结果强调，较冷的小鼠设施温度可通过激素应激途径显着增加肠道蠕动。