Sleep Loss Alters Basal Metabolic Hormone Secretion and Modulates the Dynamic Counterregulatory Response to Hypoglycemia
Abstract
Context: Sleep loss has immediate effects on metabolic function that in the long run may contribute to the development of obesity and type 2 diabetes. Objective: Our objective was to explore the neuroendocrine mechanisms mediating the acute effects of sleep deprivation on blood glucose regulation under basal and hypoglycemic conditions. Methods: In a randomized, crossover study in 10 healthy young men, plasma concentrations of relevant hormones were examined during basal rest, a subsequent stepwise hypoglycemic clamp after one night of total sleep deprivation (SD) and one night of regular sleep. Results: Basal glucagon concentrations were decreased (P = 0.022) and C-peptide levels were slightly reduced after SD (P = 0.085), compared with regular sleep. During hypoglycemia after SD, the glucagon increase relative to baseline was enhanced (P = 0.034) and the relative decrease in C-peptide was reduced (P = 0.013). Also, the relative increase in norepinephrine was reduced (P = 0.031). SD did not affect epinephrine, ACTH, cortisol, lactate, β-hydroxybutyrate, or nonesterified fatty acids during hypoglycemia, but overall, plasma nonesterified fatty acid levels were reduced after SD (P = 0.009). SD markedly increased rated hunger during basal rest (P < 0.008), resulting in a dampened relative increase during hypoglycemia (P < 0.009). Unexpectedly, despite distinct alterations in basal secretory activity, the absolute amplitude of hormonal counterregulation and hunger responses to hypoglycemia was not affected by SD. Conclusion: Short-term SD distinctly alters hormonal glucose regulation, affecting especially pancreatic islet secretion, and also increases hunger. Immediate perturbations in the dynamic regulation of energy metabolism caused by acute sleep curtailment may contribute to the association between chronic sleep loss and metabolic disorders.
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Increased fasting glucose was reported after 120 hours of total sleep deprivation but not after 72-126 hours or one night of total sleep deprivation.
“Increased fasting glucose was reported after 120 h of TSD [200] but not after 72–126 h [86] or one single night of TSD [5, 143, 195, 204]”
From Sleep and metabolic function (2012) · cites this paper as [143]
Two studies found that one night of total sleep deprivation increased subjective hunger the next morning.
“More recently, two studies [5, 143] reported that a night of TSD resulted in increased subjective hunger the following morning.”
From Sleep and metabolic function (2012) · cites this paper as [143]
Partial and total sleep deprivation result in elevated salivary and plasma cortisol the following afternoon and evening, while morning cortisol may be unchanged or decreased.
“Partial and total sleep deprivation resulted in elevated salivary and plasma cortisol the following afternoon and evening100,101,109,114,117 (Table 1), while morning cortisol levels may be unchanged or even decreased.90,97,117”
From Interacting epidemics? Sleep curtailment, insulin resistance, and obesity (2012) · cites this paper as [97]
Total and partial sleep deprivation reduce glucose tolerance in lean individuals.
“Total and partial sleep deprivation reduced glucose tolerance in lean individuals.”
From Interacting epidemics? Sleep curtailment, insulin resistance, and obesity (2012) · cites this paper as [97]
Two crossover studies of a single night of total sleep deprivation or partial sleep deprivation showed decreased basal glucagon levels, while catecholamine levels remained unchanged.
“Two crossover studies of a single night of total sleep [32] or partial sleep [30] deprivation showed decreased basal glucagon levels, however catecholamines levels remained unchanged.”
From Association between sleep deficiency and cardiometabolic disease: implications for health disparities (2016) · cites this paper as [32]
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- Authors
- Schmid, S. M., Hallschmid, M., Jauch-Chara, K., Bandorf, N., Born, J., & Schultes, B.
- Affiliations
- University of Lübeck (DE)
- Departments of Internal Medicine I (S.M.S., K.J.-C., N.B., B.S.), University of Luebeck, D-23538 Luebeck, Germany
- Department of Neuroendocrinology (M.H., J.B.), University of Luebeck, D-23538 Luebeck, Germany
- Kantonsspital St. Gallen (CH)
- Corresponding author
- Schultes, Bernd
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2007-08-01
- Volume
- 92
- Issue
- 8
- Pages
- 3044-3051
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- OpenAlex
- W2065142413
- Cited by
- 115
- References
- 38
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 5 · 2023: 2 · 2022: 2 · 2021: 4 · 2020: 7 · 2019: 5 · 2018: 8 · 2017: 2 · 2016: 4 · 2015: 10 · 2014: 6 · 2013: 12 · 2012: 10
- FWCI
- 4.16
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Keywords
- sleep deprivation, hypoglycemia, counterregulatory response, glucagon, C-peptide, norepinephrine, hunger, glucose regulation, free fatty acids, neuroendocrine regulation, type 2 diabetes, obesity
- MeSH terms
- Adrenocorticotropic Hormone, Adult, C-Peptide, Epinephrine, Fatty Acids, Nonesterified, Glucagon, Glucose, Hormones, Humans, Hunger, Hydrocortisone, Hypoglycemia, Male, Neurosecretory Systems, Norepinephrine, Sleep Deprivation, Glucose Clamp Technique, Cross-Over Studies, Lactic Acid, Human Growth Hormone, 3-Hydroxybutyric Acid
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