Department of Microbiology and Immunology, Stanford University, Stanford, CA, USA.
Buck Institute for Research on Aging, Novato, CA, USA.
Lab Anim (NY). 2024 Jun;53(6):148-159. doi: 10.1038/s41684-024-01376-5. Epub 2024 May 28.
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.
研究人员提倡将实验小鼠的饲养温度从常规的 22°C 升高到小鼠的热中性点 30°C,以提高转化研究的效率。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得到探索。在这里,我们发现饲养在 22°C 的小鼠的整个肠道传输速度几乎是饲养在 30°C 的小鼠的两倍,这主要是由于结肠传输速度增加了三倍。此外,两种温度下的肠道微生物群落组成存在差异,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 时来自下丘脑-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中起着关键作用。应激激素促肾上腺皮质激素释放激素的药理学和遗传学耗竭会减缓 22°C 应激小鼠的肠道运动,但对相对无应激的 30°C 小鼠没有类似的影响。总之,我们的研究结果表明,较冷的实验动物饲养温度通过激素应激途径显著增加了肠道运动。