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Cited by 283Sleep and related disordersRegulation of Appetite and ObesitySleep and Wakefulness Research

Role of sleep duration in the regulation of glucose metabolism and appetite

Open access
Morselli, Lisa, Leproult, Rachel, Balbo, Marcella, Spiegel, Karine·2010·Best Practice & Research Clinical Endocrinology & Metabolism
DOI 10.1016/j.beem.2010.07.005PMC PMC3018785
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Abstract

Sleep curtailment has become a common behavior in modern society. This review summarizes the current laboratory evidence indicating that sleep loss may contribute to the pathophysiology of diabetes mellitus and obesity. Experimentally induced sleep loss in healthy volunteers decreases insulin sensitivity without adequate compensation in beta-cell function, resulting in impaired glucose tolerance and increased diabetes risk. Lack of sleep also down-regulates the satiety hormone leptin, up-regulates the appetite-stimulating hormone ghrelin, and increases hunger and food intake. Taken together with the epidemiologic evidence for an association between short sleep and the prevalence or incidence of diabetes mellitus and/or obesity, these results support a role for reduced sleep duration in the current epidemic of these metabolic disorders. Screening for habitual sleep patterns in patients with "diabesity" is therefore of great importance. Studies are warranted to investigate the putative therapeutic impact of extending sleep in habitual short sleepers with metabolic disorders.

AI snapshot

Written from the paper’s full text.

TL;DR

This review summarizes laboratory evidence that sleep curtailment impairs glucose metabolism and alters appetite-regulating hormones, supporting a role for short sleep in diabetes and obesity. It argues that habitual sleep patterns should be assessed in patients with “diabesity” and that extending sleep in short sleepers warrants therapeutic investigation.

Key findings

  • Experimental sleep restriction decreases insulin sensitivity without adequate beta-cell compensation: after 5–6 nights of 4 h in bed in 11 young men, the disposition index fell by about 40%, glucose effectiveness was 30% lower, acute insulin response to glucose was reduced by more than 30%, and 3 of 11 subjects had disposition index values <1.000.
  • Sleep loss alters appetite regulation: 2 nights of 4 h vs. 10 h in bed decreased leptin by 18%, increased ghrelin by 28%, increased the ghrelin:leptin ratio by more than 70%, increased hunger by 23%, and increased appetite for high-carbohydrate nutrients by more than 30%.
  • Caloric intake rises with sleep restriction: one night of 4 h vs. 8 h in bed increased next-day caloric intake by 22%; 4 nights of 4.5 h vs. 8.5 h in bed increased intake by 14%; in women, 4 nights of ~5.5 h vs. 2 nights of ~9 h produced a 20% increase in self-reported food consumption and +0.4 kg weight gain.
  • Epidemiologic evidence links short sleep to higher prevalence or incidence of obesity/diabetes, and the review reports dose-response changes in 24-h leptin profiles and HOMA across 4-h, 8-h, and 12-h bedtime conditions.

Methods

  • Narrative review of laboratory and epidemiologic studies on sleep duration, glucose metabolism, appetite regulation, and energy expenditure, including total and partial sleep deprivation paradigms.
  • Synthesizes human studies in healthy lean, overweight, or obese adults, women, adolescents, and older long sleepers; measures include OGTT/ivGTT, hyperinsulinemic euglycemic clamp, hormone profiles, indirect calorimetry, doubly labeled water, and actigraphy.
  • Main analysis is qualitative synthesis with summary tables and figures; no new primary data or meta-analysis are presented.

Limitations

  • Stated in the paper: some findings await further confirmation; the clinical significance of glucagon results remains to be investigated; the relative contributions of circadian misalignment and sleep loss cannot be unequivocally dissected; effects in children, older adults, and patients with metabolic/endocrine disorders need documentation; therapeutic impact of bedtime extension is still to be tested.
  • Evident from the text: as a narrative review, it lacks a systematic search or meta-analysis; many cited studies are small, preliminary, or conference abstracts, and some use single-timepoint hormone assessments.
  • Evident from the text: results are contradictory across studies for leptin, physical activity, and glucose tolerance, and some negative studies had limited actual sleep-duration differences between conditions (e.g., final difference of only about 16 min).

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1016/j.beem.2010.07.005

Cites

72 of 72 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 63 cited sources checked · 0 supported · 0 flagged

  • Interpretationnone given

    Sleep loss down-regulates the satiety hormone leptin.

    “Lack of sleep also down-regulates the satiety hormone leptin, up-regulates the appetite-stimulating hormone ghrelin, and increases hunger and food intake.”
    Quote in the paperSubstantial claim
  • Interpretationreasoning

    Reduced sleep duration plays a role in the current epidemic of diabetes mellitus and obesity.

    “Taken together with the epidemiologic evidence for an association between short sleep and the prevalence or incidence of diabetes mellitus and/or obesity, these results support a role for reduced sleep duration in the current epidemic of these metabolic disorders.”
    • Also stated in: § Introduction · boosted
      “strongly suggesting that short sleep is an important, though still widely underestimated, non-traditional lifestyle factor involved in the current epidemic of diabetes and obesity.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The effects of laboratory sleep restriction paradigms generalize to habitual short sleepers with metabolic disorders and to the real-world chronic sleep curtailment that the paper links to diabetes and obesity.
  • Premisecitation

    In the only study focusing on women only, progressive sleep curtailment over 4 nights had no impact on measures of glucose tolerance and insulin sensitivity.

    “In the only study focusing on women only, no impact of progressive sleep curtailment over 4 nights was reported on measures of glucose tolerance and SI [28].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [28] Bosy-Westphal, 2008, Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women, Obes Facts source

      Not checked in the free run.

  • Premisecitation

    Fasting blood glucose levels were increased at the end of 120 hours of total sleep deprivation.

    “fasting blood glucose levels were increased at the end of the sleep deprivation period [13].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [13] Vondra, 1981, Effects of sleep deprivation on the activity of selected metabolic enzymes in skeletal muscle, Eur J Appl Physiol Occup Physiol source

      Not checked in the free run.

  • Premisecitation

    Two nights of 4h in bed versus 10h in bed increased ghrelin by 28%.

    “Overall leptin levels were decreased by 18%, while ghrelin increased by 28%, and the ghrelin:leptin ratio increased by more than 70% when sleep was restricted.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [44] Spiegel, 2004, Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite, Ann Intern Med source

      Not checked in the free run.

  • May combine two claims. 23
  • Classified as probably not a substantial claim. 6

  • May combine two claims.

    Premisecitation

    Physiological sleep need is about 9h across adolescence; US 9th-12th grade teens sleep 7h12min on school nights and French 15-19 year olds sleep 7h45min.

    “While laboratory studies have shown that physiological sleep need is about 9h across all ages of adolescence [11], sleep duration on school nights is 7h12min for 9th to 12th grade American teens [7] and 7h45min for 15-19 years old French adolescents [9].”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [11] Carskadon, 2002, Regulation of sleepiness in adolescents: update, insights, and speculation, Sleep source

      Not checked in the free run.

    • cites [7] Teens and Sleep

      Not checked in the free run.

    • cites [9] Enquête Sofrès/ISV

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Leptin levels are modulated by both sleep and circadian rhythmicity.

    “a study using an abrupt 8-h shift of bedtimes and continuous enteral nutrition to eliminate the impact of meal intake demonstrated that leptin levels are modulated by both sleep and circadian rhythmicity [40].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [40] Simon, 1998, Circadian and ultradian variations of leptin in normal man under continuous enteral nutrition: relationship to sleep and body temperature, J Clin Endocrinol Metab source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    During circadian misalignment, sleep efficiency was reduced to 67% versus 84% at baseline, and glucose and insulin responses to breakfast were increased.

    “sleep efficiency was reduced to 67% at the peak of circadian misalignment (versus 84% at baseline), and the glucose and insulin responses to breakfast were increased [35].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [35] Scheer, 2009, Adverse metabolic and cardiovascular consequences of circadian misalignment, Proc Natl Acad Sci U S A source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    In 2008, US working adults reported an average sleep need of 7h18min, an average sleep duration of 6h40min, with 44% sleeping less than 7h and 16% less than 6h on a typical week-night.

    “Data from the 2008 “Sleep in America” poll of the National Sleep Foundation indicate that although working adults report a sleep need of an average of 7h18min to function at best, the average sleep duration is 6h40min, with 44% of them sleeping less than 7h on a typical week-night (as opposed to only 15.6% in 1960 [10]), and 16% less than 6h”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [6] National Sleep Foundation

      Not checked in the free run.

    • cites [10] Kripke, 1979, Short and long sleep and sleeping pills. Is increased mortality associated?, Arch Gen Psychiatry source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Semi-chronic sleep restriction of 2 weeks of 5.5h versus 8.5h in bed in middle-aged overweight adults was associated with decreased insulin sensitivity during ivGTT without appropriate compensatory beta-cell release, resulting in reduced oral glucose tolerance.

    “semi-chronic sleep restriction (2 weeks of 5.5h versus 8.5h in bed) in middle-aged overweight adults was associated with decreased SI during ivGTT without appropriate compensatory beta-cell release, as AIRg was not affected by the sleep condition, resulting in reduced oral glucose tolerance [32].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [32] Nedeltcheva, 2009, Exposure to recurrent sleep restriction in the setting of high caloric intake and physical inactivity results in increased insulin resistance and reduced glucose tolerance, J Clin Endocrinol Metab source

      Not checked in the free run.

  • May combine two claims.

    Interpretationreasoning

    Experimentally induced sleep loss in healthy volunteers decreases insulin sensitivity without adequate compensation in beta-cell function, resulting in impaired glucose tolerance and increased diabetes risk.

    “Experimentally-induced sleep loss in healthy volunteers decreases insulin sensitivity without adequate compensation in beta-cell function, resulting in impaired glucose tolerance and increased diabetes risk.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisereasoning

    Recurrent partial sleep deprivation has become increasingly common.

    “Since then, recurrent partial sleep deprivation, i.e. the result of a voluntary behavior reflecting the demands and opportunities of modern society, has become increasingly common.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    60 hours of total sleep deprivation increased fasting insulin levels and the insulin response to an oral glucose tolerance test without changing glucose levels, suggesting insulin resistance.

    “60h of TSD in young healthy male volunteers was shown to increase fasting insulin levels, as well as the insulin response to OGTT, while no change was observed for glucose levels, suggesting that TSD induced insulin resistance [14].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [14] VanHelder, 1993, Effects of sleep deprivation and exercise on glucose tolerance, Aviat Space Environ Med

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Two nights of 4h in bed versus 10h in bed decreased glucose tolerance, partly as a result of inadequate insulin secretion.

    “Even though sleep duration was manipulated for only 2 nights, glucose tolerance was decreased, partly as a result of inadequate insulin secretion.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [25] Spiegel, 2005, Sleep loss: a novel risk factor for insulin resistance and type 2 diabetes, J Appl Physiol source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In the state of sleep debt, the disposition index was decreased by an average of about 40% compared with the fully rested state, and 3 of 11 subjects had disposition index values below 1.000, indicating high diabetes risk.

    “In the state of sleep debt, the DI was decreased by an average of about 40% as compared to the fully rested state, and 3 of the 11 subjects had DI values <1.000, indicating a high risk of diabetes [24].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [24] Xiang, 2006, Effect of pioglitazone on pancreatic beta-cell function and diabetes risk in Hispanic women with prior gestational diabetes, Diabetes source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Compared with 2 nights of 8h in bed, morning fasting glucose levels were unchanged after sleep loss while morning fasting insulin concentrations were increased, indicating reduced insulin sensitivity.

    “Compared to 2 nights of 8h in bed, morning fasting glucose levels were unchanged after sleep loss, while morning fasting insulin concentrations were increased, indicating reduced SI.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [34] van Leeuwen, 2010, Prolonged sleep restriction affects glucose metabolism in healthy young men, Int J Endocrinol

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Eight nights of 5h bedtimes after a baseline period of 10h bedtimes resulted in a 40% decrease in insulin sensitivity without adequate compensation by insulin release and a markedly decreased disposition index.

    “Preliminary findings indicate that, following sleep restriction, the subjects experienced a 40% decrease in SI, without adequate compensation by insulin release. The DI was thus markedly decreased after sleep loss [26].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [26] Leproult R & Van Cauter E. Marked decreased insulin sensitivity and increased evening cortisol levels following one week of partial sleep deprivation. 12th meeting of the European NeuroEndocrine Association (ENEA) 2006. Athens, Greece.

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    In France, adults aged 18 to 55 years reported an average work-night sleep duration of 6h58min, and 33% slept less than 7h per night.

    “a survey conducted in France among adults aged 18 to 55 years reported that, on work-nights, the average sleep duration was 6h58min and that 33% of the respondents slept less than 7h per night”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [8] Enquête

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Insulin and leptin appear to negatively modulate the food rewarding system, whereas ghrelin exerts opposite effects.

    “Furthermore, insulin and leptin appear to negatively modulate the food rewarding system [67], whereas ghrelin exerts opposite effects [68]; the changes in these hormonal concentrations following sleep restriction could therefore contribute to the increased hedonic, rather than homeostatic, eating, that may be typical of short sleepers.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [67] Davis, 2010, Insulin, leptin and reward, Trends Endocrinol Metab source

      Not checked in the free run.

    • cites [68] Lutter, 2009, Homeostatic and hedonic signals interact in the regulation of food intake, J Nutr source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In healthy overweight subjects, 14 nights of 5.5h in bed compared to 14 nights of 8.5h did not affect total energy expenditure, resting metabolic rate, or the thermic effect of food.

    “In a protocol involving a more prolonged sleep restriction (14 nights of 5.5h vs. 14 nights of 8.5h in bed) in healthy overweight subjects, total EE assessed by the gold standard doubly labeled water method, resting metabolic rate assessed by indirect calorimetry, and the thermic effect of food were not affected by the bedtime condition [48].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [48] Nedeltcheva, 2009, Sleep curtailment is accompanied by increased intake of calories from snacks, Am J Clin Nutr source

      Not checked in the free run.

  • May combine two claims.

    Premiseown data

    HOMA levels post-breakfast increased from the 12-h to the 4-h in bed condition, indicating a decrease in glucose tolerance and/or a decrease in insulin sensitivity proportional to the severity of sleep loss.

    “HOMA levels post-breakfast increased from the 12-h to the 4-h in bed condition indicating a decrease in glucose tolerance and/or a decrease in SI proportional to the severity of sleep loss (Figure 2; panels A).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [19] Spiegel, 2004, Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin, J Clin Endocrinol Metab source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Two studies observed increased, rather than decreased, morning leptin levels after sleep restriction even when food intake was similar in both sleep conditions; sleep restriction did not result in changes in hunger, appetite or satiety.

    “However, two studies observed increased, rather than decreased, morning leptin levels after sleep restriction even food intake was similar in both sleep conditions; sleep restriction did not result in changes in hunger, appetite or satiety [34, 52].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [34] van Leeuwen, 2010, Prolonged sleep restriction affects glucose metabolism in healthy young men, Int J Endocrinol

      Not checked in the free run.

    • cites [52] Omisade, 2010, Impact of acute sleep restriction on cortisol and leptin levels in young women, Physiol Behav source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Obesity is a major risk factor for diabetes mellitus and is crucial in the pathogenesis of sleep-disordered breathing (SDB), a reported independent risk factor for insulin resistance.

    “Finally, obesity is in itself a major risk factor for diabetes mellitus and has been shown to be crucial in the pathogenesis of sleep-disordered breathing (SDB), a reported independent risk factor for insulin resistance [73].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [73] Spiegel, 2009, Effects of poor and short sleep on glucose metabolism and obesity risk, Nat Rev Endocrinol source

      Not checked in the free run.

    • Rests on an assumption: Obesity is a major risk factor for diabetes mellitus.

  • May combine two claims.

    Interpretationcitation

    Sleep loss is associated with increased levels of proinflammatory cytokines and low-grade inflammation, a condition that may predispose to insulin and leptin resistance.

    “Furthermore, sleep loss is associated with increased levels of proinflammatory cytokines and low-grade inflammation (reviewed in chapter 9 “Sleep loss and inflammation”), a condition that may predispose to insulin [69-71] and leptin resistance [72].”
    Quote in the paperSubstantial claim0 of 4 sources checked
    • cites [69] Vgontzas, 2004, Adverse effects of modest sleep restriction on sleepiness, performance, and inflammatory cytokines, J Clin Endocrinol Metab source

      Not checked in the free run.

    • cites [70] van Leeuwen, 2009, Sleep restriction increases the risk of developing cardiovascular diseases by augmenting proinflammatory responses through IL-17 and CRP, PLoS One source

      Not checked in the free run.

    • cites [71] Meier-Ewert, 2004, Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk, J Am Coll Cardiol source

      Not checked in the free run.

    • cites [72] Chen, 2006, Induction of leptin resistance through direct interaction of C-reactive protein with leptin, Nat Med source

      Not checked in the free run.

  • May combine two claims.

    Interpretationcitation

    The only three studies that examined the impact of behavioral sleep restriction on physical activity have yielded contradictory results; the possible involvement of reduced activity-related EE in the link between short sleep and increased obesity risk remains to be determined.

    “The only three studies that examined the impact of behavioral sleep restriction on physical activity have yielded contradictory results; the possible involvement of reduced activity-related EE in the link between short sleep and increased obesity risk remains to be determined.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

    Interpretationnone given

    Reduced energy expenditure during sleep loss could represent another mechanism contributing to the link between short sleep and increased weight consistently reported in epidemiologic studies.

    “Beside the changes in neurohormones involved in the regulation of food intake, reduced energy expenditure (EE) during sleep loss could represent another mechanism contributing to the link between short sleep and increased weight consistently reported in epidemiologic studies.”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: Short sleep is associated with increased weight/obesity in epidemiologic studies.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationcitation

    A shift towards the morning of the nocturnal elevation of leptin levels may have occurred due to shifted short bedtimes, resulting in higher morning leptin levels.

    “As the nocturnal elevation in leptin levels is influenced both by sleep and circadian rhythmicity [40], a shift towards the morning of the nocturnal elevation of leptin levels may have occurred due to the shifted short bedtimes, resulting in higher morning leptin levels.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [40] Simon, 1998, Circadian and ultradian variations of leptin in normal man under continuous enteral nutrition: relationship to sleep and body temperature, J Clin Endocrinol Metab source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationown data

    Sleep duration affects multiple facets of normal human physiology.

    “Figure 2 illustrates the fact that sleep duration affect multiple facets of normal human physiology.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationreasoning

    From evidence obtained so far, short sleep appears to affect energy balance because of an up-regulation of orexigenic hormones and a downregulation of anorexigenic hormones associated with increased hunger and caloric intake, rather than because of a reduced energy expenditure.

    “Thus, from evidence obtained so far, it appears that short sleep affects energy balance because of an up-regulation of orexigenic hormones and a downregulation of anorexigenic hormones associated with increased hunger and caloric intake, rather than because of a reduced EE.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    Compared to a fully rested night (8-10 h in bed), satiety was reduced and levels of PYY were lower in the sleep loss condition.

    “Compared to a fully rested night (8-10 h in bed), satiety was reduced and levels of PYY, an anorexigenic peptide produced by the gastrointestinal tract in response to food intake, were lower in the sleep loss condition.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [53] Magee, 2009, Acute sleep restriction alters neuroendocrine hormones and appetite in healthy male adults, Sleep Biol Rhythms source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In young women, 4 nights of about 5.5h sleep versus 2 nights of about 9h sleep with an ad libitum diet increased self-reported food consumption by 20% and produced weight gain of 0.4 kg.

    “when young women were exposed to an ad libitum diet during 2 bedtime conditions, ie 4 nights of ∼ 5.5h of sleep vs. 2 nights of ∼ 9h of sleep, a 20% increase in self-reported food consumption was observed in the sleep restriction condition and weight gain (+0.4kg) occurred [28].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [28] Bosy-Westphal, 2008, Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women, Obes Facts source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Leptin secretion is inhibited by sympathetic activity and ghrelin secretion is inhibited by parasympathetic activity.

    “Since leptin secretion is inhibited by sympathetic activity [65] and ghrelin secretion is inhibited by parasympathetic activity [66], the changes in the activity of autonomic nervous system observed with sleep loss may be involved in the simultaneous reduction of leptin and increase of ghrelin.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [65] Rayner, 2001, Regulation of leptin production: sympathetic nervous system interactions, J Mol Med source

      Not checked in the free run.

    • cites [66] van der Lely, 2004, Biological, physiological, pathophysiological, and pharmacological aspects of ghrelin, Endocr Rev source

      Not checked in the free run.

27 of 27

  • The paper relies on this without support.

    The effects of laboratory sleep restriction paradigms generalize to habitual short sleepers with metabolic disorders and to the real-world chronic sleep curtailment that the paper links to diabetes and obesity.

    “Studies are warranted to investigate the putative therapeutic impact of extending sleep in habitual short sleepers with metabolic disorders.”

  • The paper relies on this without support.

    Short sleep is associated with increased weight/obesity in epidemiologic studies.

    “the link between short sleep and increased weight consistently reported in epidemiologic studies”

  • The paper relies on this without support.

    The brain is a major user of glucose.

    “considering that brain is a major user of glucose”

  • The paper relies on this without support.

    Sympathetic activation inhibits insulin release, and parasympathetic activation stimulates insulin release.

    “Sympathetic activation inhibits, and para-sympathetic activation stimulates, insulin release”

  • The paper relies on this without support.

    Sleep loss is associated with sleepiness and fatigue.

    “Sleep loss is associated with sleepiness and fatigue”

  • The paper relies on this without support.

    Obesity is a major risk factor for diabetes mellitus.

    “obesity is in itself a major risk factor for diabetes mellitus”
6 of 6

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Laboratory findings show that physiologic sleep loss is associated with diabetes risk factors, including insulin resistance, and other diabetes risk factors, such as increased consumption of unhealthy foods.

    “These studies are supported by laboratory findings that show that physiologic sleep loss is associated with diabetes risk factors, including insulin resistance,53–56 and other diabetes risk factors, such as increased consumption of unhealthy foods.57–59”

    From Sleep, Health, and Society (2017) · cites this paper as [54]

Cites

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Related

Authors
Morselli, L., Leproult, R., Balbo, M., & Spiegel, K.
Affiliations
  • University of Chicago (US)
  • Azienda Ospedaliera Nazionale SS. Antonio e Biagio e Cesare Arrigo (IT)
  • Lyon 1 Université (FR)
Corresponding author
Spiegel, Karine
ORCID
Venue
Best Practice & Research Clinical Endocrinology & Metabolism
Publisher
Elsevier BV
Published
2010-10
Volume
24
Issue
5
Pages
687-702
ISSN
1521-690X (ISSN-L)
DOI
10.1016/j.beem.2010.07.005
PMC
PMC3018785
OpenAlex
W2126361281
Cited by
283
References
80
Citations by year
2026: 9 · 2025: 13 · 2024: 14 · 2023: 23 · 2022: 18 · 2021: 24 · 2020: 20 · 2019: 17 · 2018: 18 · 2017: 20 · 2016: 14 · 2015: 18 · 2014: 19 · 2013: 28 · 2012: 19
FWCI
2.23
Type
journal article
Language
en
Open access
Licence
Locations
  • Best Practice & Research Clinical Endocrinology & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion)
Funders
  • U.S. Department of Defense
  • National Institutes of Health
  • National Institute on Aging (P01-AG11412., P01AG011412)
  • National Heart, Lung, and Blood Institute (R01HL075079, R01HL075025)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK071696, P60DK20595, R01 DK0716960, P60DK020595)
  • National Center for Research Resources (M01RR000055)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (P50HD057796)
Topics
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
Keywords
sleep duration, sleep deprivation, glucose metabolism, insulin sensitivity, beta-cell function, impaired glucose tolerance, diabetes mellitus, obesity, leptin, ghrelin, appetite, dietary intake, diabesity, sleep screening
MeSH terms
Appetite Regulation, Diabetes Mellitus, Type 2, Energy Metabolism, Glucose, Humans, Obesity, Sleep, Sleep Deprivation, Time Factors

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