Skeletal muscle insulin sensitivity show circadian rhythmicity which is independent of exercise training status
Open accessAbstract
Circadian rhythms can be perturbed by shift work, travel across time zones, occupational tasks, or genetic mutations. Perturbed circadian rhythms are associated with the increasing problem of obesity, metabolic dysfunction and insulin resistance. We hypothesized that insulin sensitivity in skeletal muscle follows a circadian pattern and that this pattern is important for overall metabolic function. This hypothesis was verified using mice as a model system. We observed circadian rhythmicity in whole body insulin tolerance, as well as in signaling pathways regulating insulin- and exercise-induced glucose uptake in skeletal muscle, including AKT, 5'-adenosine monophosphate-activated protein kinase (AMPK) and TBC1 domain family member 4 (TBC1D4) phosphorylation. Basal and insulin-stimulated glucose uptake in skeletal muscle and adipose tissues in vivo also differed between day- and nighttime. However, the rhythmicity of glucose uptake differed from the rhythm of whole-body insulin tolerance. These results indicate that neither skeletal muscle nor adipose tissue play a major role for the circadian rhythmicity in whole-body insulin tolerance. To study the circadian pattern of insulin sensitivity directly in skeletal muscle, we determined glucose uptake under basal and submaximal insulin-stimulated conditions ex vivo every sixth hour. Both insulin sensitivity and signaling of isolated skeletal muscle peaked during the dark period. We next examined the effect of exercise training on the circadian rhythmicity of insulin sensitivity. As expected, voluntary exercise training enhanced glucose uptake in skeletal muscle. Nevertheless, exercise training did not affect the circadian rhythmicity of skeletal muscle insulin sensitivity. Taken together, our results provide evidence that skeletal muscle insulin sensitivity exhibits circadian rhythmicity.
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Hypercortisolism induced by chronic stress, Cushing's syndrome, or medication is a known risk factor for the development of diabetes.
“For instance, hypercortisolism induced by chronic stress, Cushing’s syndrome, or medication is a known risk factor for the development of diabetes.”
From Mathematical Modelling of Endocrine Systems (2019) · cites this paper as [81]
The Introduction discusses diurnal changes in glucose tolerance and insulin sensitivity, not hypercortisolism as a diabetes risk factor. Searches for chronic stress, Cushing’s syndrome, medication, cortisol, and glucocorticoids found no passage in our copy addressing the claimed risk. (LLM, conf=0.76)
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Милованова, К. Г., Zakharova, A. N., Орлова, А. А., Kollantay, O. V., Shuvalov, I. Y., Popov, S. A., Medvedev, M. A., Kovalev, I. V., Yakimovich, I. Y., Chibalin, A., et al. (2025) · Bulletin of Siberian Medicine · doi:10.20538/1682-0363-2024-4-82-94
Timing the strain: skeletal muscle clock as regulator of physical activity
Kawano, I., & Asher, G. (2026) · npj Metabolic Health and Disease · doi:10.1038/s44324-026-00121-5
The clock‐output gene DBP regulates muscle insulin sensitivity and its fluctuations
Yodokawa, C., Kajimura, Y., Taguchi, A., Hiroshige, S., Nagao, Y., Akiyama, M., Yodokawa, T., Masuda, K., Mikami, H., Tanizawa, Y., et al. (2026) · Journal of Diabetes Investigation · doi:10.1111/jdi.70481
- Authors
- Basse, A. L., Dalbram, E., Larsson, L., Gerhart-Hines, Z., Zierath, J. R., & Treebak, J. T.
- Affiliations
- University of Copenhagen (DK)
- Corresponding author
- Treebak, Jonas T.
- Venue
- Frontiers in Physiology
- Publisher
- Frontiers Media SA
- Published
- 2018-08-28
- Volume
- 9
- Pages
- 1198-1198
- ISSN
- 1664-042X (ISSN-L)
- PMC
- PMC6121032
- OpenAlex
- W2889056797
- Cited by
- 52
- References
- 37
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 6 · 2023: 4 · 2022: 8 · 2021: 4 · 2020: 10 · 2019: 6 · 2018: 1
- FWCI
- 2.96
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Physiology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Novo Nordisk Fonden (14OC0011493, 14OC0009315)
- Det Frie Forskningsråd (4004-00235)
- European Foundation for the Study of Diabetes (EFSD/Lilly Research Fellowship)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- circadian rhythm, skeletal muscle insulin sensitivity, insulin tolerance, glucose uptake, exercise training, AMPK, Akt, TBC1D4, adipose tissue, insulin signaling, circadian rhythm disruption, insulin resistance
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