THE SIGNIFICANCE OF SLEEP IN GLUCOSE METABOLISM REGULATION – THE ROLE OF CIRCADIAN RHYTHM DISRUPTIONS IN TYPE 2 DIABETES DEVELOPMENT: A NARRATIVE REVIEW

Background: Sleep and circadian rhythm disturbances constitute modifiable risk factors for type 2 diabetes mellitus (T2DM). Meta-analytic evidence demonstrates that short sleep duration (<6h/night) increases T2DM risk by 28–33% (OR 1.28–1.33), while shift work elevates incidence by 9–40% (RR 1.09–1.40). Aims: The aim of this narrative review is to synthesise current epidemiological, interventional, and mechanistic evidence on how sleep disturbances and circadian rhythm disruptions influence type 2 diabetes pathophysiology in adults. Methods: A structured narrative review was conducted using literature from PubMed, Scopus, Web of Science, and Google Scholar (2015–2025). Searches employed terms: "sleep duration glucose metabolism", "circadian rhythm type 2 diabetes", "clock genes insulin resistance", "shift work diabetes risk", "melatonin glucose homeostasis". Meta-analyses, systematic reviews, cohort studies, and randomized controlled trials were included. Results: Epidemiological evidence reveals a U-shaped sleep–T2DM relationship with optimal risk at 7–8 hours/night. Short sleep (<6h) and long sleep (>9h) both increase T2DM risk (OR 1.28–1.48). Night shift work elevates risk dose-dependently (RR 1.40, 95% CI 1.15–1.71) across 1.16 million participants. Molecular mechanisms involve desynchronized clock genes (CLOCK, BMAL1, PER2, CRY1), mitochondrial dysfunction reducing oxidative capacity 20–30%, and altered melatonin signaling. Sleep extension interventions improve insulin sensitivity 17–45% within 1 week. Evening chronotherapy with glucose-lowering drugs demonstrates superior efficacy compared to morning dosing. CBT-I (cognitive behavioral therapy for insomnia) reduces T2DM incidence by 42% in prediabetic populations. Conclusion: Sleep and circadian optimization represent cost-effective, modifiable strategies for T2DM prevention. Personalized chronotherapy guided by genetic profiling and objective sleep/activity monitoring warrants implementation in clinical practice and public health policies.

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Publication Details

Journal
International Journal of Innovative Technologies in Social Science
Published
2026-01-28
DOI
https://doi.org/10.31435/ijitss.1(49).2026.4632
Primary Topic
Circadian rhythm and melatonin
Type
article
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article

THE SIGNIFICANCE OF SLEEP IN GLUCOSE METABOLISM REGULATION – THE ROLE OF CIRCADIAN RHYTHM DISRUPTIONS IN TYPE 2 DIABETES DEVELOPMENT: A NARRATIVE REVIEW

Wiktoria Błaszczyk, Anastasiia D. Holoborodko, Anhelina Loputs, Bartosz Lautenbach et al.
International Journal of Innovative Technologies in Social Science
Circadian rhythm and melatonin
article

THE SIGNIFICANCE OF SLEEP IN GLUCOSE METABOLISM REGULATION – THE ROLE OF CIRCADIAN RHYTHM DISRUPTIONS IN TYPE 2 DIABETES DEVELOPMENT: A NARRATIVE REVIEW

Wiktoria Błaszczyk, Anastasiia D. Holoborodko, Anhelina Loputs, Bartosz Lautenbach, Ewa Wieczorkiewicz, Agnieszka Pocheć, Eliza Garbacz, Patrycja Stępińska, Klaudia Wojciech, Dariusz Nędza
article en

Abstract

Background: Sleep and circadian rhythm disturbances constitute modifiable risk factors for type 2 diabetes mellitus (T2DM). Meta-analytic evidence demonstrates that short sleep duration (<6h/night) increases T2DM risk by 28–33% (OR 1.28–1.33), while shift work elevates incidence by 9–40% (RR 1.09–1.40). Aims: The aim of this narrative review is to synthesise current epidemiological, interventional, and mechanistic evidence on how sleep disturbances and circadian rhythm disruptions influence type 2 diabetes pathophysiology in adults. Methods: A structured narrative review was conducted using literature from PubMed, Scopus, Web of Science, and Google Scholar (2015–2025). Searches employed terms: "sleep duration glucose metabolism", "circadian rhythm type 2 diabetes", "clock genes insulin resistance", "shift work diabetes risk", "melatonin glucose homeostasis". Meta-analyses, systematic reviews, cohort studies, and randomized controlled trials were included. Results: Epidemiological evidence reveals a U-shaped sleep–T2DM relationship with optimal risk at 7–8 hours/night. Short sleep (<6h) and long sleep (>9h) both increase T2DM risk (OR 1.28–1.48). Night shift work elevates risk dose-dependently (RR 1.40, 95% CI 1.15–1.71) across 1.16 million participants. Molecular mechanisms involve desynchronized clock genes (CLOCK, BMAL1, PER2, CRY1), mitochondrial dysfunction reducing oxidative capacity 20–30%, and altered melatonin signaling. Sleep extension interventions improve insulin sensitivity 17–45% within 1 week. Evening chronotherapy with glucose-lowering drugs demonstrates superior efficacy compared to morning dosing. CBT-I (cognitive behavioral therapy for insomnia) reduces T2DM incidence by 42% in prediabetic populations. Conclusion: Sleep and circadian optimization represent cost-effective, modifiable strategies for T2DM prevention. Personalized chronotherapy guided by genetic profiling and objective sleep/activity monitoring warrants implementation in clinical practice and public health policies.

International Journal of Innovative Technologies in Social Science(1(49))
Medical University of Lublin (PL), Medical University of Silesia (PL), Jan Kochanowski University (PL), Indiana University Hospital (US), Leibniz Association (DE), Antoni Jurasz University Hospital (PL), Andrzej Frycz Modrzewski Krakow University (PL), Łukasiewicz Research Network - Institute of Welding (PL), University of Silesia in Katowice (PL)
Good health and well-being
Openalex Percentile: Top 71%
Circadian rhythm and melatonin
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