Circadian Desynchrony Promotes Metabolic Disruption in a Mouse Model of Shiftwork
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Shiftwork is associated with adverse metabolic pathophysiology, and the rising incidence of shiftwork in modern societies is thought to contribute to the worldwide increase in obesity and metabolic syndrome. The underlying mechanisms are largely unknown, but may involve direct physiological effects of nocturnal light exposure, or indirect consequences of perturbed endogenous circadian clocks. This study employs a two-week paradigm in mice to model the early molecular and physiological effects of shiftwork. Two weeks of timed sleep restriction has moderate effects on diurnal activity patterns, feeding behavior, and clock gene regulation in the circadian pacemaker of the suprachiasmatic nucleus. In contrast, microarray analyses reveal global disruption of diurnal liver transcriptome rhythms, enriched for pathways involved in glucose and lipid metabolism and correlating with first indications of altered metabolism. Although altered food timing itself is not sufficient to provoke these effects, stabilizing peripheral clocks by timed food access can restore molecular rhythms and metabolic function under sleep restriction conditions. This study suggests that peripheral circadian desynchrony marks an early event in the metabolic disruption associated with chronic shiftwork. Thus, strengthening the peripheral circadian system by minimizing food intake during night shifts may counteract the adverse physiological consequences frequently observed in human shift workers.
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Night eating syndrome in humans and a shift of food intake from the active phase to the rest phase in laboratory rodents have been associated with adverse metabolic consequences.
“The night eating syndrome in humans (33,34) and a shift of food intake from the active phase to the rest phase in laboratory rodents (35,36) have been associated with adverse metabolic consequences.”
From Circadian Misalignment Augments Markers of Insulin Resistance and Inflammation, Independently of Sleep Loss (2014) · cites this paper as [36]
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Self-citation
- Authors
- Barclay, J. L., Husse, J., Bode, B., Naujokat, N., Meyer-Kovac, J., Schmid, S. M., Lehnert, H., & Oster, H.
- Affiliations
- Max Planck Institute for Biophysical Chemistry (DE)
- University of Lübeck (DE)
- Corresponding author
- Oster, Henrik
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-05-21
- Volume
- 7
- Issue
- 5
- Pages
- e37150
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3357388
- OpenAlex
- W2104310168
- Cited by
- 259
- References
- 53
- Citations by year
- 2026: 9 · 2025: 11 · 2024: 15 · 2023: 13 · 2022: 15 · 2021: 19 · 2020: 19 · 2019: 18 · 2018: 21 · 2017: 21 · 2016: 20 · 2015: 24 · 2014: 26 · 2013: 24 · 2012: 4
- FWCI
- 11.13
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- Deutsche Forschungsgemeinschaft (SFB654)
- Volkswagen Foundation
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Health Sciences › Medicine › Physiology › Dietary Effects on Health
- Keywords
- shift work, circadian desynchrony, metabolic disruption, sleep restriction, peripheral circadian clock, suprachiasmatic nucleus, glucose metabolism, lipid metabolism, metabolic syndrome, obesity, nocturnal light exposure, feeding behavior
- MeSH terms
- Animals, Biological Clocks, Circadian Rhythm, Disease Models, Animal, Eating, Gene Expression Regulation, Liver, Male, Suprachiasmatic Nucleus, Sleep Disorders, Circadian Rhythm, Mice, Transcriptome
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