Temperature-dependent differences in mouse gut motility are mediated by stress

  • Lab Anim (NY). 2024 Jun;53(6):148-159. doi: 10.1038/s41684-024-01376-5.
Alvin Han  1 ,  Courtney Hudson-Paz  2 ,  Beatriz G Robinson  3 ,  Laren Becker  4 ,  Amanda Jacobson  5 ,  Julia A Kaltschmidt  6 ,  Jennifer L Garrison  2  7 ,  Ami S Bhatt  8  9 ,  Denise M Monack  10
Affiliations
  • 1. Department of Microbiology and Immunology, Stanford University, Stanford, CA, USA.
  • 2. Buck Institute for Research on Aging, Novato, CA, USA.
  • 3. Neurosciences IDP Graduate Program, Stanford University School of Medicine, Stanford, CA, USA.
  • 4. Department of Medicine (Gastroenterology and Hepatology), Stanford University, Stanford, CA, USA.
  • 5. Genentech Inc., Research and Early Development, Immunology Discovery, South San Francisco, CA, USA.
  • 6. Department of Neurosurgery, Stanford University School of Medicine, Stanford, CA, USA.
  • 7. Global Consortium for Reproductive Longevity & Equality, Novato, CA, USA.
  • 8. Department of Medicine (Hematology, Blood and Marrow Transplantation), Stanford University, Stanford, CA, USA. [email protected].
  • 9. Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA. [email protected].
  • 10. Department of Microbiology and Immunology, Stanford University, Stanford, CA, USA. [email protected].
PMID: 38806681 DOI: 10.1038/s41684-024-01376-5
Abstract

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.

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