Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Alerts
  • Advertising/recruitment
  • Subscribe
  • Contact
  • Current Issue
  • Past Issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • Tumor Microenvironment (Mar 2021)
    • 100th Anniversary of Insulin's Discovery (Jan 2021)
    • Hypoxia-inducible factors in disease pathophysiology and therapeutics (Oct 2020)
    • Latency in Infectious Disease (Jul 2020)
    • Immunotherapy in Hematological Cancers (Apr 2020)
    • Big Data's Future in Medicine (Feb 2020)
    • Mechanisms Underlying the Metabolic Syndrome (Oct 2019)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Commentaries
    • Concise Communication
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • In-Press Preview
  • Commentaries
  • Concise Communication
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Alerts
  • Advertising/recruitment
  • Subscribe
  • Contact
Adrenal glucocorticoids have a key role in circadian resynchronization in a mouse model of jet lag
Silke Kiessling, … , Gregor Eichele, Henrik Oster
Silke Kiessling, … , Gregor Eichele, Henrik Oster
Published June 23, 2010
Citation Information: J Clin Invest. 2010;120(7):2600-2609. https://doi.org/10.1172/JCI41192.
View: Text | PDF
Research Article

Adrenal glucocorticoids have a key role in circadian resynchronization in a mouse model of jet lag

  • Text
  • PDF
Abstract

Jet lag encompasses a range of psycho- and physiopathological symptoms that arise from temporal misalignment of the endogenous circadian clock with external time. Repeated jet lag exposure, encountered by business travelers and airline personnel as well as shift workers, has been correlated with immune deficiency, mood disorders, elevated cancer risk, and anatomical anomalies of the forebrain. Here, we have characterized the molecular response of the mouse circadian system in an established experimental paradigm for jet lag whereby mice entrained to a 12-hour light/12-hour dark cycle undergo light phase advancement by 6 hours. Unexpectedly, strong heterogeneity of entrainment kinetics was found not only between different organs, but also within the molecular clockwork of each tissue. Manipulation of the adrenal circadian clock, in particular phase-shifting of adrenal glucocorticoid rhythms, regulated the speed of behavioral reentrainment. Blocking adrenal corticosterone either prolonged or shortened jet lag, depending on the time of administration. This key role of adrenal glucocorticoid phasing for resetting of the circadian system provides what we believe to be a novel mechanism-based approach for possible therapies for jet lag and jet lag–associated diseases.

Authors

Silke Kiessling, Gregor Eichele, Henrik Oster

×

Figure 6

MET injection prior to jet lag affects behavioral resetting kinetics in a phase-delay paradigm.

Options: View larger image (or click on image) Download as PowerPoint
MET injection prior to jet lag affects behavioral resetting kinetics in ...
After injection of MET or saline for 16 days, animals were released into an 8-hour phase delay paradigm. (A and B) Representative double-plotted actograms of SALD and METD mice (A) and SALN and METN mice (B) 2 weeks before and 2 weeks after 8-hour phase delay of the LD cycle. Time and duration of MET treatment is shown by red bars. Dark phases are denoted by gray shading. (C and D) Resetting kinetics of activity onsets of METD and SALD mice (C) and METN and SALN mice (D). The curves of injected animals differed significantly from that of saline-treated control animals (P < 0.0001, METD vs. SALD and METN vs. SALN; n = 6 per group). Differences between MET- and saline-injected animals were still significant (P = 0.0105) when the shift was shortened to 7 hours, caused by delayed onset after MET injection at ZT12. All values are average ± SEM.

Copyright © 2021 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts