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Glucocorticoid regulation of the circadian clock modulates glucose homeostasis
Open accessAbstract
Circadian clock genes are regulated by glucocorticoids; however, whether this regulation is a direct or secondary effect and the physiological consequences of this regulation were unknown. Here, we identified glucocorticoid response elements (GREs) at multiple clock genes and showed that 3 were directly regulated by the glucocorticoid receptor. We determined that a GRE within the core clock gene Per2 was continuously occupied during rhythmic expression and essential for glucocorticoid regulation of that gene in vivo. We further demonstrated that mice with a genomic deletion spanning this GRE expressed elevated leptin levels and were protected from glucose intolerance and insulin resistance on glucocorticoid treatment but not from muscle wasting. We conclude that Per2 is an integral component of a particular glucocorticoid regulatory pathway and that glucocorticoid regulation of the peripheral clock is selectively required for some actions of glucocorticoids.
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“Resetting of the peripheral clock occurs through well-defined molecular mechanisms that involve direct interaction of glucocorticoids, glucocorticoid response elements and the regulatory regions of core clock genes Bmal1, Cry1, Per1 and Per2 [63, 64].”
From Sleep, testosterone and cortisol balance, and ageing men (2022) · cites this paper as [64]
Experimental — accuracy not yet measuredIn the citing paper
“Per2 null mice exhibit no glucocorticoid oscillations, indicating that PER2 may also impact glucocorticoid receptor (GR)-dependent glucose metabolism [24,25].”
From Circadian control of glucose metabolism (2014) · cites this paper as [24]
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BackgroundInsulin Controls Clock Gene Expression in the Liver of Goldfish Probably via Pi3k/Akt Pathway
Sáiz, N., Velasco, C., de Pedro, N., Soengas, J. L., & Isorna, E. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241511897 · Cited by 6
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Zhu, B. (2022) · Physiology · doi:10.1152/physiol.00003.2022 · Cited by 4
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Dexamethasone is a regulator of clock genes in testicular peritubular cells
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“Glucocorticoids such as corticosterone bind to GR, which in turn anchor in the GRE or GBS in the promoter region of Per1 and Per2 and other clock genes to activate their transcriptions (Balsalobre et al., 2000; Cheon et al., 2013; Dickmeis et al., 2013; Oster et al., 2017; So et al., 2009).”
InfluentialDifferential Expression of Circadian Clock Genes in the Bovine Neuroendocrine Adrenal System
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“According to Chun et al. [32], increased amounts of PER1 mRNA is potentially related to the ability of peripheral molecular clocks to adapt to environmental stimuli such as stress due to the presence of glucocorticoid response elements in the promoter sequence of the PER1 gene [35].”
BackgroundFibroblasts as an in vitro model of circadian genetic and genomic studies
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“For the known circadian transcription factors, HOMER identified significant enrichment of the binding sequences for BMAL1 (p = 1e-29), NPAS2 (p = 1e-9), CLOCK (p = 1e-10), particularly within regions that had increasing accessibility over time.”
BackgroundInfluentialStress and the Central Circadian Clock
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Effects of Psychosocial Stress on the Gene Expression of the Clock Genes hPER1 and hPER2 in Humans
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“In Per2, there could be 8 different identified Glucocorticoid binding sites (GBS’s) of which one seems to be constantly occupied during Per2’s rhythmic expression and is furthermore essential for the regulation of glucocorticoids (So et al., 2009).”
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“The Per2 gene contains a glucocorticoid-responsive element that is important in glucose homeostasis (5), and hyperglycemia downregulates expression of Per2 (6), giving the authors solid ground on which to base the current work.”
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“After dexamethasone binds to glucocorticoid receptors, ligand-receptor complexes translocate to the nucleus; then, these bind to the glucocorticoid response elements (GREs) on the promoters of core clock genes, such as Per1 and Per2, thereby directly activating the core clock machinery (So et al. 2009; Cheon et al. 20…”
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Hypertension-induced metabolic dysregulation drives multi-organ circadian desynchrony in rats
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Metadata
- Authors
- So, A. Y.-L., Bernal, T. U., Pillsbury, M. L., Yamamoto, K. R., & Feldman, B. J.
- Affiliations
- University of California, San Francisco (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2009-10-13
- Volume
- 106
- Issue
- 41
- Pages
- 17582-17587
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2757402
- OpenAlex
- W1998522501
- Cited by
- 431
- References
- 51
- Citations by year
- 2026: 15 · 2025: 26 · 2024: 37 · 2023: 19 · 2022: 36 · 2021: 28 · 2020: 32 · 2019: 28 · 2018: 22 · 2017: 28 · 2016: 33 · 2015: 23 · 2014: 25 · 2013: 20 · 2012: 18
- FWCI
- 8.68
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- University of California, San Francisco
- National Cancer Institute (CA20535, R01CA020535, R37CA020535)
- National Institute of General Medical Sciences (R25GM056847, GM 56847)
- National Institute of Diabetes and Digestive and Kidney Diseases (K08DK073697, DK73697)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- glucocorticoids, circadian clock, clock genes, glucocorticoid response element, glucocorticoid receptor, Per2, glucose homeostasis, insulin resistance, impaired glucose tolerance, leptin, muscle atrophy, peripheral clocks
- MeSH terms
- Animals, Circadian Rhythm, Gene Expression Regulation, Glucocorticoids, Glucose, Homeostasis, Nuclear Proteins, Transcription Factors, Transcription, Genetic, Polymerase Chain Reaction, Cell Cycle Proteins, Leptin, Mice, Period Circadian Proteins, Mesenchymal Stem Cells
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