Sleep loss: a novel risk factor for insulin resistance and type 2 diabetes
Abstract
Chronic sleep loss as a consequence of voluntary bedtime restriction is an endemic condition in modern society. Although sleep exerts marked modulatory effects on glucose metabolism, and molecular mechanisms for the interaction between sleeping and feeding have been documented, the potential impact of recurrent sleep curtailment on the risk for diabetes and obesity has only recently been investigated. In laboratory studies of healthy young adults submitted to recurrent partial sleep restriction, marked alterations in glucose metabolism including decreased glucose tolerance and insulin sensitivity have been demonstrated. The neuroendocrine regulation of appetite was also affected as the levels of the anorexigenic hormone leptin were decreased, whereas the levels of the orexigenic factor ghrelin were increased. Importantly, these neuroendocrine abnormalities were correlated with increased hunger and appetite, which may lead to overeating and weight gain. Consistent with these laboratory findings, a growing body of epidemiological evidence supports an association between short sleep duration and the risk for obesity and diabetes. Chronic sleep loss may also be the consequence of pathological conditions such as sleep-disordered breathing. In this increasingly prevalent syndrome, a feedforward cascade of negative events generated by sleep loss, sleep fragmentation, and hypoxia are likely to exacerbate the severity of metabolic disturbances. In conclusion, chronic sleep loss, behavioral or sleep disorder related, may represent a novel risk factor for weight gain, insulin resistance, and Type 2 diabetes.
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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 [48]
Controlled laboratory studies have repeatedly found large decreases in insulin sensitivity among young adults after sleep loss.
“Several well-controlled laboratory studies have consistently shown marked reductions in insulin sensitivity in young adults following sleep loss [2–7].”
From Sleep restriction increases free fatty acids in healthy men (2015) · cites this paper as [3]
Short-term, acute, laboratory, and cross-sectional observational studies indicate that adverse changes in sleep are associated with adverse changes in insulin and glucose response but can be reversed when sleep quantity and quality are restored.
“Short-term, acute, laboratory, and cross-sectional observational studies indicate that adverse changes in sleep are associated with adverse changes in insulin and glucose response but can be reversed when sleep quantity and quality are restored.78”
From Sleep duration and incidence of obesity in infants, children, and adolescents: a systematic review and meta-analysis of prospective studies (2018) · cites this paper as [78]
Insufficient sleep duration is associated with weight gain and obesity.
“short sleep duration (6 hours or less), and especially very short sleep duration (less than 5 hours) is associated with increased cardiometabolic morbidity and mortality, including weight gain and obesity, hypertension, hyperlipidemia, and diabetes.”
From Sleep: important considerations for the prevention of cardiovascular disease (2016) · cites this paper as [29]
Insufficient sleep is linked to lower energy expenditure, altered glucose homeostasis, and alterations in hormones that mediate hunger.
“insufficient sleep has been linked to lower energy expenditure, altered glucose homeostasis and alterations in hormones that mediate hunger(24, 25, 27-31).”
From Sleep: important considerations for the prevention of cardiovascular disease (2016) · cites this paper as [29]
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 [56]
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.”
From Role of sleep duration in the regulation of glucose metabolism and appetite (2010) · cites this paper as [25]
In humans, transient misalignment of behaviors and the circadian clock increases inflammation and impairs glucose regulation, with potential relevance to cardiovascular disease.
“In humans, transient misalignment of behaviors and the circadian clock increases inflammation and impairs glucose regulation (137-140), with potential relevance to CV disease (141).”
From Role of the circadian system in cardiovascular disease (2018) · cites this paper as [139]
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Self-citationSleep Restriction for 1 Week Reduces Insulin Sensitivity in Healthy Men
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Self-citationInsomnia With Objective Short Sleep Duration Is Associated With Type 2 Diabetes
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Self-citationSelf-Reported Sleep Duration is Associated with the Metabolic Syndrome in Midlife Adults
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Self-citationSleep and Circadian Rhythms in Humans
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Self-citationObstructive Sleep Apnea and Metabolic Syndrome: Alterations in Glucose Metabolism and Inflammation
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Self-citationSelf-reported sleep quality is associated with the metabolic syndrome
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Self-citationObstructive sleep apnoea and type 2 diabetes mellitus: a bidirectional association
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Self-citationShift work and cancer – considerations on rationale, mechanisms, and epidemiology
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- Authors
- Spiegel, K., Knutson, K., Leproult, R., Tasali, E., & Cauter, E. V.
- Affiliations
- Université Libre de Bruxelles (BE)
- University of Chicago (US)
- Venue
- Journal of Applied Physiology
- Publisher
- American Physiological Society
- Published
- 2005-11
- Volume
- 99
- Issue
- 5
- Pages
- 2008-2019
- ISSN
- 0161-7567 (ISSN-L)
- 8750-7587
- 1522-1601
- OpenAlex
- W2115361864
- Cited by
- 1,175
- References
- 119
- Citations by year
- 2026: 20 · 2025: 31 · 2024: 37 · 2023: 42 · 2022: 43 · 2021: 50 · 2020: 43 · 2019: 56 · 2018: 54 · 2017: 64 · 2016: 62 · 2015: 68 · 2014: 75 · 2013: 81 · 2012: 67
- FWCI
- 8.98
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Applied Physiology (publishedVersion)
- PubMed (publishedVersion)
- Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion)
- Funders
- National Center for Research Resources (P41RR013642)
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Keywords
- sleep deprivation, chronic sleep restriction, insulin resistance, type 2 diabetes, glucose metabolism, glucose tolerance, leptin, ghrelin, appetite regulation, obesity, sleep-disordered breathing, hypoxia, sleep fragmentation, short sleep duration
- MeSH terms
- Diabetes Mellitus, Type 2, Glucaric Acid, Humans, Insulin Resistance, Risk Factors, Sympathetic Nervous System, Vagus Nerve, Sleep Apnea, Obstructive
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