Cited by 1,006Regulation of Appetite and ObesitySleep and Wakefulness ResearchCircadian rhythm and melatonin

Leptin Levels Are Dependent on Sleep Duration: Relationships with Sympathovagal Balance, Carbohydrate Regulation, Cortisol, and Thyrotropin

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Spiegel, Karine, Leproult, Rachel, L’Hermite-Balériaux, Mireille, Copinschi, Georges, Penev, Plamen D., Van Cauter, Eve·2004·The Journal of Clinical Endocrinology & Metabolism

Abstract

Sleep plays an important role in energy homeostasis. The present study tests the hypothesis that circulating levels of leptin, a hormone that signals energy balance to the brain, are influenced by sleep duration. We also analyzed associations between leptin and sympathovagal balance, cortisol, TSH, glucose, and insulin under different bedtime conditions. Twenty-four-hour hormonal and glucose profiles were sampled at frequent intervals, and sympathovagal balance was estimated from heart rate variability in 11 subjects studied after 6 d of 4-h bedtimes (mean +/- sem of sleep duration during last 2 d: 3 h and 49 +/- 2 min) and after 6 d of 12-h bedtimes (sleep: 9 h and 03 +/- 15 min). A study with 8-h bedtimes was performed 1 yr later (sleep: 6 h and 52 +/- 10 min). Caloric intake and activity levels were carefully controlled in all studies. Mean levels, maximal levels, and rhythm amplitude of leptin were decreased (-19%, -26%, and -20%, respectively) during sleep restriction compared with sleep extension. The decrease in leptin levels was concomitant with an elevation of sympathovagal balance. The effects of sleep duration on leptin were quantitatively associated with alterations of the cortisol and TSH profiles and were accompanied by an elevation of postbreakfast homeostasis model assessment values. Measures of perceived stress were not increased during sleep restriction. During the study with 8-h bedtimes, hormonal and metabolic parameters were intermediate between those observed with 4-h and 12-h bedtimes. In conclusion, sleep modulates a major component of the neuroendocrine control of appetite.

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Crossref · 10.1210/jc.2004-1003

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  • Sleep loss from acute total sleep deprivation or severe recurrent sleep restriction (≤5 h/night) results in elevated evening cortisol levels, often with a slower decline of cortisol concentrations across the day.

    “sleep loss, resulting from either acute total sleep deprivation or severe recurrent sleep restriction (≤5, 5 h/ night) resulted in elevated evening cortisol levels, often associated with a slower decline of cortisol concentrations across the day.[8][9][10][11][12][13][14][15][16][17]”

    From Effects of Insufficient Sleep on Pituitary–Adrenocortical Response to CRH Stimulation in Healthy Men (2017) · cites this paper as [10]

    The Experimental protocol describes six nights with four hours in bed, and the cortisol findings report higher late-afternoon and evening levels and a slower decline during restriction than during sleep extension (page numbers unavailable). The copy does not establish that acute total sleep deprivation produced those cortisol effects; its discussion of acute total deprivation concerns leptin and TSH. (LLM, conf=0.86)

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  • Reduced leptin is implicated as a hormonal mechanism by which sleep restriction can worsen insulin sensitivity, increase circulating lipids, and lead to obesity and abdominal obesity via disruption of energy balance and increased cravings for carbohydrate rich foods.

    “These data implicate reduced leptin as a hormonal mechanism by which sleep restriction can worsen insulin sensitivity, increase circulating lipids, and lead to obesity and abdominal obesity via disruption of energy balance and increased cravings for carbohydrate rich foods.”

    From Impact of Five Nights of Sleep Restriction on Glucose Metabolism, Leptin and Testosterone in Young Adult Men (2012) · cites this paper as [17]

    Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

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  • Sleep restriction is linked with obesity via disruption of leptin and increased cravings for carbohydrate rich foods.

    “This prompted the hypothesis that sleep restriction is linked with obesity via disruption of leptin and increased cravings for carbohydrate rich foods [17].”

    From Impact of Five Nights of Sleep Restriction on Glucose Metabolism, Leptin and Testosterone in Young Adult Men (2012) · cites this paper as [17]

    The Discussion (page unavailable) reports that sleep restriction lowers leptin and may adversely affect appetite regulation; it also describes the evidence linking shorter sleep with obesity as suggestive. It does not report increased cravings specifically for carbohydrate-rich foods. The carbohydrate-rich meals mentioned in the Experimental protocol were provided to participants, not foods they reported craving. (LLM, conf=0.87)

    Experimental — accuracy not yet measured
  • 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 [47]

    The Discussion (page unavailable) reports altered cortisol regulation and sympathovagal balance after sleep restriction, alongside impaired morning glucose tolerance. It does not explicitly propose either pathway as a mediator of the glucose impairment; the reported changes are concomitant. (LLM, conf=0.82)

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  • Severe sleep restriction results in elevated evening cortisol levels.

    “Severe sleep restriction results in elevated evening cortisol levels.”

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1 of the 69 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. Buxton OM, Spiegel K, Van Cauter E 2002 Chapter 8: Modulation of endocrine function and metabolism by sleep and sleep loss. In: Lee-Chiong TL, Sateia MJ, Carskadon MA, eds. Sleep Medicine. Handley, Philadelphia: Belfus, Inc.; 59 -69

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Authors
Spiegel, K., Leproult, R., L’Hermite-Balériaux, M., Copinschi, G., Penev, P. D., & Van Cauter, E.
Affiliations
  • Université Libre de Bruxelles (BE)
  • University of Chicago (US)
Venue
The Journal of Clinical Endocrinology & Metabolism
Published
2004-11
Volume
89
Issue
11
Pages
5762-5771
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
OpenAlex
W2115505164
Cited by
1,006
References
69
Citations by year
2026: 18 · 2025: 29 · 2024: 28 · 2023: 52 · 2022: 48 · 2021: 40 · 2020: 50 · 2019: 30 · 2018: 42 · 2017: 41 · 2016: 57 · 2015: 57 · 2014: 61 · 2013: 78 · 2012: 74
FWCI
9.76
Type
journal article
Language
en
Open access
Locations
  • The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion, other-oa)
  • Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion)
Funders
  • University of Chicago
  • National Institutes of Health
  • National Institute on Aging (P01AG011412, AG-11412)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK 20595, DK-41814, R01DK041814)
  • National Center for Research Resources (M01-RR 00055, M01RR000055)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
Keywords
leptin, sleep duration, sleep restriction, sleep extension, sympathovagal balance, heart rate variability, cortisol, thyroid-stimulating hormone, glucose, insulin, HOMA, carbohydrate regulation, energy homeostasis, appetite regulation, neuroendocrine regulation, perceived stress
MeSH terms
Adult, Homeostasis, Humans, Hydrocortisone, Male, Sleep, Sympathetic Nervous System, Thyrotropin, Time Factors, Vagus Nerve, Leptin, Carbohydrate Metabolism

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