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Connecting insufficient sleep and insomnia with metabolic dysfunction
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The global epidemic of obesity and type 2 diabetes parallels the rampant state of sleep deprivation in our society. Epidemiological studies consistently show an association between insufficient sleep and metabolic dysfunction. Mechanistically, sleep and circadian rhythm exert considerable influences on hormones involved in appetite regulation and energy metabolism. As such, data from experimental sleep deprivation in humans demonstrate that insufficient sleep induces a positive energy balance with resultant weight gain, due to increased energy intake that far exceeds the additional energy expenditure of nocturnal wakefulness, and adversely impacts glucose metabolism. Conversely, animal models have found that sleep loss–induced energy expenditure exceeds caloric intake resulting in net weight loss. However, animal models have significant limitations, which may diminish the clinical relevance of their metabolic findings. Clinically, insomnia disorder and insomnia symptoms are associated with adverse glucose outcomes, though it remains challenging to isolate the effects of insomnia on metabolic outcomes independent of comorbidities and insufficient sleep durations. Furthermore, both pharmacological and behavioral interventions for insomnia may have direct metabolic effects. The goal of this review is to establish an updated framework for the causal links between insufficient sleep and insomnia and risks for type 2 diabetes and obesity.
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“Interventions may also address insufficient sleep and chronic stress, which can negatively affect appetite and metabolism.65”
From Obesity Management in Adults: A Review (2023) · cites this paper as [65]
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Metadata
- Authors
- Duan, D., Kim, L. J., Jun, J. C., & Polotsky, V. Y.
- Affiliations
- Johns Hopkins University (US)
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2022-11-13
- Volume
- 1519
- Issue
- 1
- Pages
- 94-117
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- PMC
- PMC9839511
- OpenAlex
- W4308953898
- Cited by
- 110
- References
- 213
- Citations by year
- 2026: 43 · 2025: 35 · 2024: 20 · 2023: 12
- FWCI
- 2.44
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annals of the New York Academy of Sciences (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Heart Association (Postdoctoral Fellowship Award 828142)
- American Academy of Sleep Medicine Foundation (273‐BS‐22)
- National Institute of Diabetes and Digestive and Kidney Diseases (K23DK133690)
- National Heart, Lung, and Blood Institute (5T32HL110952, R01HL128970, R01HL13310, R01HL135483, R61HL156240, U18DA052301)
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Keywords
- insufficient sleep, insomnia, sleep deprivation, metabolic dysfunction, type 2 diabetes, obesity, circadian rhythm, appetite regulation, energy balance, glucose metabolism, energy expenditure
- MeSH terms
- Diabetes Mellitus, Type 2, Energy Metabolism, Humans, Sleep Initiation and Maintenance Disorders, Obesity, Sleep, Sleep Deprivation
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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