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Cited by 448Circadian rhythm and melatoninPancreatic function and diabetesSleep and Work-Related Fatigue

Modulation of glucose regulation and insulin secretion by circadian rhythmicity and sleep

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Van Cauter, E, Blackman, J D, Roland, D, Spire, J P, Refetoff, S, Polonsky, K S·1991·Journal of Clinical Investigation
DOI 10.1172/jci115396
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Abstract

To define the roles of circadian rhythmicity (intrinsic effects of time of day independent of the sleep or wake condition) and sleep (intrinsic effects of the sleep condition, irrespective of the time of day) on the 24-h variation in glucose tolerance, eight normal men were studied during constant glucose infusion for a total of 53 h. The period of study included 8 h of nocturnal sleep, 28 h of continuous wakefulness, and 8 h of daytime sleep. Blood samples for the measurement of glucose, insulin, C-peptide, cortisol, and growth hormone were collected at 20-min intervals throughout the entire study. Insulin secretion rates were derived from C-peptide levels by deconvolution. Sleep was polygraphically monitored. During nocturnal sleep, levels of glucose and insulin secretion increased by 31 +/- 5% and 60 +/- 11%, respectively, and returned to baseline in the morning. During sleep deprivation, glucose levels and insulin secretion rose again to reach a maximum at a time corresponding to the beginning of the habitual sleep period. The magnitude of the rise above morning levels averaged 17 +/- 5% for glucose and 49 +/- 8% for calculated insulin secretion. Serum insulin levels did not parallel the circadian variation in insulin secretion, indicating the existence of an approximate 40% increase in insulin clearance during the night. Daytime sleep was associated with a 16 +/- 3% rise in glucose levels, a 55 +/- 7% rise in insulin secretion, and a 39 +/- 5% rise in serum insulin. The diurnal variation in insulin secretion was inversely related to the cortisol rhythm, with a significant correlation of the magnitudes of their morning to evening excursions. Sleep-associated rises in glucose correlated with the amount of concomitant growth hormone secreted. These studies demonstrate previously underappreciated effects of circadian rhythmicity and sleep on glucose levels, insulin secretion, and insulin clearance, and suggest that these effects could be partially mediated by cortisol and growth hormone.

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  • Both the hypothalamic-pituitary-adrenal axis and the autonomic nervous system pathways have been proposed as possible mediators of the impairments in glucose tolerance associated with sleep restriction.

    “Both these pathways also have been proposed as possible mediators of the impairments in glucose tolerance associated with sleep restriction (22,44–48).”

    From Sleep Restriction for 1 Week Reduces Insulin Sensitivity in Healthy Men (2010) · cites this paper as [45]

    The Discussion (page not specified) proposes cortisol as a possible mediator of diurnal variation in glucose tolerance, including observations made during 28 hours of sleep deprivation. It does not propose an autonomic nervous system pathway as a mediator, or attribute the glucose-tolerance changes specifically to sleep restriction rather than circadian rhythmicity. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Under normally entrained conditions, glucose tolerance, b-cell responsivity, and insulin sensitivity peak in the morning and deteriorate as the day progresses.

    “Previous highly controlled laboratory experimental studies have reported that under normally entrained conditions (i.e., sleep at night and evening dinner), glucose tolerance, b-cell responsivity, and insulin sensitivity peak in the morning and deteriorate as the day progresses (31).”

    From Interplay of Dinner Timing and <i>MTNR1B</i> Type 2 Diabetes Risk Variant on Glucose Tolerance and Insulin Secretion: A Randomized Crossover Trial (2022) · cites this paper as [31]

    The Introduction and Discussion report poorer glucose tolerance in the afternoon and evening than in the morning and identify diminished insulin sensitivity and insufficient insulin secretion as contributors. But this study used constant glucose infusion, not an evening dinner, and did not directly measure β-cell responsivity as such. The cited paper therefore supports the diurnal pattern but not all of the stated conditions and measures. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • During sleep deprivation, glucose and insulin elevations are about half the amplitude of those during nocturnal sleep, indicating that circadian-dependent processes also modulate glucose regulation.

    “A glucose and insulin elevation of roughly half the amplitude of the one observed during nocturnal sleep was apparent during the night of sleep deprivation, indicating that circadian-dependent processes also modulate glucose regulation.”

    From Sleep and metabolic function (2012) · cites this paper as [187]

  • The 24-hour cortisol profile is only modestly affected by the presence or absence of sleep.

    “As shown in Fig. 1b, this profile is only modestly affected by the presence or absence of sleep.”

    From Sleep and metabolic function (2012) · cites this paper as [187]

  • Growth hormone levels increase during sleep regardless of when sleep occurs and are markedly reduced during sleep deprivation.

    “GH levels are increased during sleep, irrespective of the time at which sleep occurs, and they are markedly diminished during sleep deprivation.”

    From Sleep and metabolic function (2012) · cites this paper as [187]

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Authors
Van Cauter, E., Blackman, J. D., Roland, D., Spire, J. P., Refetoff, S., & Polonsky, K. S.
Affiliations
Université Libre de Bruxelles (BE)
ORCID
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1991-09-01
Volume
88
Issue
3
Pages
934-942
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci115396
OpenAlex
W2127903745
Cited by
448
References
33
Citations by year
2026: 11 · 2025: 8 · 2024: 21 · 2023: 19 · 2022: 24 · 2021: 19 · 2020: 36 · 2019: 24 · 2018: 17 · 2017: 15 · 2016: 21 · 2015: 20 · 2014: 21 · 2013: 12 · 2012: 26
FWCI
2.63
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed (publishedVersion)
  • Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion)
Funders
  • University of Chicago
  • National Institutes of Health
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK-31842, DK 20595, DK-41814, R01DK041814)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
Keywords
circadian rhythm, sleep, glucose regulation, insulin secretion, glucose tolerance, sleep deprivation, cortisol, growth hormone, insulin clearance, C-peptide
MeSH terms
Insulin Secretion, Adult, Blood Glucose, Circadian Rhythm, Humans, Hydrocortisone, Insulin, Male, Sleep, Growth Hormone

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