Review Article | Published:

Effects of poor and short sleep on glucose metabolism and obesity risk

Nature Reviews Endocrinology volume 5, pages 253261 (2009) | Download Citation

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Abstract

The importance of sleep to hormones and glucose metabolism was first documented more than four decades ago. Since then, sleep curtailment has become an endemic behavior in modern society. In addition, the prevalence of sleep disorders, particularly obstructive sleep apnea (OSA), has increased. OSA is very common in endocrine and metabolic disorders, but often remains undiagnosed. This Review summarizes the laboratory and epidemiologic evidence that suggests how sleep loss, either behavioral or disease-related, and poor quality of sleep might promote the development of obesity and diabetes mellitus, and exacerbate existing endocrine conditions. Treatment of sleep disorders has the potential to improve glucose metabolism and energy balance. Screening for habitual sleep patterns and OSA might be critically important for patients with endocrine and metabolic disorders.

Key points

  • Sleep loss, be it behavioral or related to sleep disorders, is an increasingly common condition in modern society

  • Experimental reduction of the duration or quality of sleep has a deleterious effect on glucose metabolism

  • Experimental reduction of sleep duration downregulates the satiety hormone, leptin, upregulates the appetite-stimulating hormone, ghrelin, and increases hunger and appetite

  • Numerous cross-sectional and prospective, epidemiologic studies have provided evidence of an association between short-duration and/or poor-quality sleep and the prevalence or incidence of diabetes mellitus or obesity

  • Effective treatment of obstructive sleep apnea, a sleep disorder that is highly prevalent in metabolic and endocrine disorders, has the potential to improve glucose metabolism and energy balance

  • Screening for habitual sleep patterns and obstructive sleep apnea might be critically important for patients with endocrine and metabolic disorders

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Acknowledgements

Some research described in this article was supported by US National Institute of Health grants P01 AG-11412, R01 HL-075079, P60 DK-20595, R01 DK-0716960, R01 HL-075025 and M01 RR000055, by US Department of Defense award W81XWH-07-2-0071, by AASM/Pfizer Scholars Grant in Sleep Medicine (E Tasali), by Belgian 'Fonds de la Recherche Scientifique Médicale' (FRSM-3.4583.02), 'Fonds National de la Recherche Scientifique' (FNRS) and 'CARE Foundation' grants, by INSERM U628, and by Claude Bernard University of Lyon, France.

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Affiliations

  1. INSERM/UCBL—U628, Integrated Physiology of Brain Arousal Systems, Lyon, France.

    • Karine Spiegel
  2. Department of Medicine, University of Chicago, Chicago, IL, USA.

    • Esra Tasali
    • , Rachel Leproult
    •  & Eve Van Cauter

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Competing interests

Eve Van Cauter has declared associations with the following companies: Actelyon (consultant) and Sanofi-Aventis (consultant). The other authors declared no competing interests.

Corresponding author

Correspondence to Karine Spiegel.

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DOI

https://doi.org/10.1038/nrendo.2009.23

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