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The metabolic burden of sleep loss
Abstract
In parallel with the increasing prevalence of obesity and type 2 diabetes, sleep loss has become common in modern societies. An increasing number of epidemiological studies show an association between short sleep duration, sleep disturbances, and circadian desynchronisation of sleep with adverse metabolic traits, in particular obesity and type 2 diabetes. Furthermore, experimental studies point to distinct mechanisms by which insufficient sleep adversely affects metabolic health. Changes in the activity of neuroendocrine systems seem to be major mediators of the detrimental metabolic effects of insufficient sleep, through favouring neurobehavioural outcomes such as increased appetite, enhanced sensitivity to food stimuli, and, ultimately, a surplus in energy intake. The effect of curtailed sleep on physical activity and energy expenditure is less clear, but changes are unlikely to outweigh increases in food intake. Although long-term interventional studies proving a cause and effect association are still scarce, sleep loss seems to be an appealing target for the prevention, and probably treatment, of metabolic disease.
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“Several observational studies have reported cross-sectional associations between inadequate sleep and greater prevalence of diabetes or impaired glucose tolerance (see [177] for another recent review).”
From Association between sleep deficiency and cardiometabolic disease: implications for health disparities (2016) · cites this paper as [177]
In the citing paper
“NREM sleep is associated with increased insulin sensitivity and glucose uptake in peripheral tissues.”
From Hypoglycemia Unawareness—A Review on Pathophysiology and Clinical Implications (2024) · cites this paper as [33]
In the citing paper
“Disruptions in sleep architecture can disrupt glucose homeostasis, predisposing individuals to hypoglycemic episodes [ 33 , 34 ].”
From Hypoglycemia Unawareness—A Review on Pathophysiology and Clinical Implications (2024) · cites this paper as [33]
In the citing paper
“Although sleep loss or a short sleep duration has negative effects on glucose metabolism, appetite, and hunger [ 31 , 32 , 33 ], sleep loss after repeated hypoglycemia could prevent hypoglycemia unawareness.”
From Hypoglycemia Unawareness—A Review on Pathophysiology and Clinical Implications (2024) · cites this paper as [33]
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Metadata
- Authors
- Schmid, S. M., Hallschmid, M., & Schultes, B.
- Affiliations
- University of Cambridge (GB)
- German Center for Diabetes Research (DE)
- eSwiss Medical and Surgical Center (CH)
- Corresponding author
- Schultes, Bernd
- Venue
- The Lancet Diabetes & Endocrinology
- Publisher
- Elsevier BV
- Published
- 2015-01
- Volume
- 3
- Issue
- 1
- Pages
- 52-62
- ISSN
- 2213-8587 (ISSN-L)
- OpenAlex
- W2145872904
- Semantic Scholar
- 847eb961d53b9fc39ac9795ecbe6de700a8252fc
- Cited by
- 328
- References
- 103
- Citations by year
- 2026: 8 · 2025: 35 · 2024: 24 · 2023: 17 · 2022: 33 · 2021: 28 · 2020: 32 · 2019: 29 · 2018: 30 · 2017: 23 · 2016: 29 · 2015: 28
- FWCI
- 4.06
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Lancet Diabetes & Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Site cant be reached (submittedVersion)
- Funders
- European Society of Endocrinology
- Deutsche Forschungsgemeinschaft (SFB 654)
- Bundesministerium für Bildung und Forschung
- Helmholtz Association
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Keywords
- sleep deprivation, short sleep duration, sleep disorders, obesity, type 2 diabetes, metabolic health, neuroendocrine system, appetite, dietary intake, energy expenditure, physical activity, sleep interventions
- MeSH terms
- Appetite, Eating, Glucose, Humans, Neurosecretory Systems, Obesity, Sleep Wake Disorders, Metabolic Syndrome
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