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A Single Night of Partial Sleep Deprivation Induces Insulin Resistance in Multiple Metabolic Pathways in Healthy Subjects
Abstract
BACKGROUND: Subsequent nights with partial sleep restriction result in impaired glucose tolerance, but the effects on insulin sensitivity have not been characterized. OBJECTIVE: The aim of this study was to evaluate the effect of a single night of partial sleep restriction on parameters of insulin sensitivity. RESEARCH DESIGN AND METHODS: Nine healthy subjects (five men, four women) were studied once after a night of normal sleep duration (sleep allowed from 2300 to 0730 h), and once after a night of 4 h of sleep (sleep allowed from 0100 to 0500 h). Sleep characteristics were assessed by polysomnography. Insulin sensitivity was measured by hyperinsulinemic euglycemic clamp studies (from 1130 to 1430 h) with infusion of [6,6-(2)H(2)]glucose. RESULTS: Sleep duration was shorter in the night with sleep restriction than in the unrestricted night (226 +/- 11 vs. 454 +/- 9 min; P< 0.0001). Sleep restriction did not affect basal levels of glucose, nonesterified fatty acids, insulin, or endogenous glucose production. Sleep restriction resulted in increased endogenous glucose production during the hyperinsulinemic clamp study compared to the unrestricted night (4.4 +/- 0.3 vs. 3.6 +/- 0.2 micromol x kg lean body mass(-1) x min(-1); P = 0.017), indicating hepatic insulin resistance. In addition, sleep restriction decreased the glucose disposal rate during the clamp (32.5 +/- 3.6 vs. 40.7 +/- 5.1 micromol x kg lean body mass(-1) x min(-1); P = 0009), reflecting decreased peripheral insulin sensitivity. Accordingly, sleep restriction decreased the rate of glucose infusion by approximately 25% (P = 0.001). Sleep restriction increased plasma nonesterified fatty acid levels during the clamp study (68 +/- 5 vs. 57 +/- 4 micromol/liter; P = 0.005). CONCLUSIONS: Partial sleep deprivation during only a single night induces insulin resistance in multiple metabolic pathways in healthy subjects. This physiological observation may be of relevance for variations in glucoregulation in patients with type 1 and type 2 diabetes.
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“Early studies reported little change in circulating insulin with sleep restriction [18], [22], but subsequent studies have found that insulin increases [15], [16], [20], particularly after breakfast [16].”
From Impact of Five Nights of Sleep Restriction on Glucose Metabolism, Leptin and Testosterone in Young Adult Men (2012) · cites this paper as [15]
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In the citing paper
“well-controlled laboratory studies in healthy adults have shown that repeated partial sleep restriction has adverse effects on systemic insulin sensitivity and glucose tolerance”
From Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction: A Randomized, Crossover Study (2012) · cites this paper as [13]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“a number of studies have found that sleep restriction does not increase overall mean cortisol [15], [16], [21], [45], [53]”
From Impact of Five Nights of Sleep Restriction on Glucose Metabolism, Leptin and Testosterone in Young Adult Men (2012) · cites this paper as [15]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Consistent with previous research [15], [18]–[20], this study found that glucose tolerance to meals was impaired and insulin increased following sleep restriction”
From Impact of Five Nights of Sleep Restriction on Glucose Metabolism, Leptin and Testosterone in Young Adult Men (2012) · cites this paper as [15]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
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“To our knowledge, this finding identifies for the first time a molecular mechanism that may be involved in the reduction in total body insulin sensitivity consistently observed in multiple laboratory studies of partial sleep deprivation in healthy adults (11–17), as well as in the participants of our study.”
From Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction: A Randomized, Crossover Study (2012) · cites this paper as [13]
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“Both reduced leptin levels (32, 33) and elevated free fatty acid concentrations (13) have been observed in healthy persons after experimental sleep restriction and could conceivably contribute to increased risk for obesity and diabetes.”
From Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction: A Randomized, Crossover Study (2012) · cites this paper as [13]
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“Fasting free fatty acids (FFA) show no significant change after one night of sleep restriction [15] and increase following two [16] nights of sleep restriction to 4 h TIB.”
From Impact of Five Nights of Sleep Restriction on Glucose Metabolism, Leptin and Testosterone in Young Adult Men (2012) · cites this paper as [15]
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“Overall insulin resistance has generally been found to worsen with sleep restriction [15], [23].”
From Impact of Five Nights of Sleep Restriction on Glucose Metabolism, Leptin and Testosterone in Young Adult Men (2012) · cites this paper as [15]
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In the citing paper
“fasting FFA were unchanged after one night of sleep restriction [15]”
From Impact of Five Nights of Sleep Restriction on Glucose Metabolism, Leptin and Testosterone in Young Adult Men (2012) · cites this paper as [15]
In the citing paper
“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 [7]
In the citing paper
“Two other studies [41, 194] reported only a decrease in SI, with apparent preservation of glucose tolerance.”
From Sleep and metabolic function (2012) · cites this paper as [41]
In the citing paper
“Small-scale experimental studies have shown that short-term sleep deprivation may lead to metabolic dysregulation[29-34], elevated inflammation[35, 36], and elevated blood pressure[37].”
From Habitual sleep duration associated with self-reported and objectively determined cardiometabolic risk factors (2014) · cites this paper as [31]
In the citing paper
“The authors observed a reduction in glucose infusion and disposal rates, indicating a deterioration of glucose tolerance and peripheral SI.”
From Role of sleep duration in the regulation of glucose metabolism and appetite (2010) · cites this paper as [33]
In the citing paper
“a number of laboratory studies examining the impact of circadian and/or sleep disruption on glucose homeostasis under controlled conditions, support the above mentioned epidemiological findings [144–147].”
From Circadian control of glucose metabolism (2014) · cites this paper as [147]
In the citing paper
“Acute partial sleep restriction of 4 hours in bed for one night when compared with a night of unrestricted sleep showed an increase in endogenous glucose production (p=0.017) and a decrease in glucose disposal rate (p=0.009) from a hyperinsulinemic clamp assessment indicating a decrease in hepatic and peripheral insulin sensitivities [22].”
From Association between sleep deficiency and cardiometabolic disease: implications for health disparities (2016) · cites this paper as [22]
In the citing paper
“Sleep restriction to 4 h TIB compared to 8.5 h TIB resulted in increased endogenous glucose production assessed by euglycemic hyperinsulinemic clamp, indicating hepatic insulin resistance [34].”
From Metabolic effects of sleep disruption, links to obesity and diabetes (2014) · cites this paper as [34]
In the citing paper
“Additionally, sleep restriction decreased glucose disposal rate during the clamp, reflecting decreased peripheral insulin sensitivity.”
From Metabolic effects of sleep disruption, links to obesity and diabetes (2014) · cites this paper as [34]
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“5 h) is able to impair glucose metabolism (10), although another study found no such effect after 4 days of gradually increasing sleep restriction (11).”
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“This has also been found in sleep restriction and sleep deprivation studies (Donga et al., 2010; Reynolds et al., 2012; Schmid et al., 2011).”
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“In addition, melatonin stimulates glucagon release from pancreatic α-cells (Gottlieb et al. 2005; Donga et al. 2010).”
BackgroundInsulin and Growth Hormone Balance: Implications for Obesity
Huang, Z., Huang, L., Waters, M. J., & Chen, C. (2020) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2020.04.005 · Cited by 88
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“In addition, increased cortisol levels and sympathetic tonus (Spiegel et al., 1999), reduced glucose clearance and increased insulin resistance (Donga et al., 2010) have been found in short-term sleep restriction laboratory studies.”
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“In this regard, previous studies reported that sleep restriction or fragmentation leads to insulin resistance in rodents (4, 14, 66) and humans (13, 15, 22, 35, 46, 58).”
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“Similar results have been found in other studies with various study designs and cohorts (Buxton et al., 2010; Donga et al., 2010; Reynolds et al., 2012; Sweeney, Jeromson, Hamilton, Brooks, & Walshe, 2017; Wang, Greer, Porter, Kaur, & Youngstedt, 2016).”
ResultCedernaes, J., Lampola, L., Axelsson, E. K., Liethof, L., Hassanzadeh, S., Yeganeh, A., Broman, J., Schiöth, H. B., & Benedict, C. (2015) · Journal of Sleep Research · doi:10.1111/jsr.12340 · Cited by 69
Metadata
- Authors
- Donga, E., van Dijk, M., van Dijk, J. G., Biermasz, N. R., Lammers, G.-J., van Kralingen, K. W., Corssmit, E. P. M., & Romijn, J. A.
- Affiliations
- Leiden University Medical Center (NL)
- Departments of Endocrinology and Metabolic Diseases (E.D., M.v.D., N.R.B., E.P.M.C., J.A.R.), Leiden University Medical Center, 2300 RC Leiden, The Netherlands
- Neurology (J.G.v.D., G.-J.L.), Leiden University Medical Center, 2300 RC Leiden, The Netherlands
- Pulmonology (K.W.v.K.), Leiden University Medical Center, 2300 RC Leiden, The Netherlands
- Corresponding author
- Donga, Esther
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2010-06-01
- Volume
- 95
- Issue
- 6
- Pages
- 2963-2968
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- OpenAlex
- W2116276541
- Cited by
- 387
- References
- 32
- Citations by year
- 2026: 22 · 2025: 17 · 2024: 16 · 2023: 24 · 2022: 24 · 2021: 23 · 2020: 21 · 2019: 36 · 2018: 29 · 2017: 22 · 2016: 24 · 2015: 30 · 2014: 25 · 2013: 28 · 2012: 23
- FWCI
- 30.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Leiden Repository (Leiden University) (submittedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Funders
- European Foundation for the Study of Diabetes
- Universiteit Leiden
- Diabetes Fonds
- Leids Universitair Medisch Centrum
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Keywords
- sleep restriction, insulin resistance, insulin sensitivity, endogenous glucose production, hepatic insulin resistance, glucose disposal rate, free fatty acids, glucose infusion rate, hyperinsulinemic-euglycemic clamp, glucose metabolism, glucoregulation, type 2 diabetes, type 1 diabetes
- MeSH terms
- Adult, Blood Glucose, Fatty Acids, Nonesterified, Female, Humans, Insulin Resistance, Liver, Male, Middle Aged, Motor Activity, Sleep Deprivation, Glucose Clamp Technique, Signal Transduction, Polysomnography
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