Trial reportThe Journal of clinical endocrinology and metabolism2015
Subchronic sleep restriction causes tissue-specific insulin resistance.
Trial report in The Journal of clinical endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
80 citing papers in PubMed, 1 synthesis or guideline pooled it, 153 citations in OpenAlex.
- A meta-analysis of the relationship between polycystic ovary syndrome and sleep disturbances risk.Frontiers in physiology · 2022Pooled it
- Sleep Extension Improves Sleep Health but Not Insulin Sensitivity in People With Overweight or Obesity Who Maintain Habitual Short Sleep Schedules.Diabetes care · 2026Trial
- Acute impairments in glucose tolerance following one night of partial sleep restriction are not rescued by moderate-intensity walking in young men.European journal of applied physiology · 2026Trial
- Effect of sleep restriction on insulin sensitivity and energy metabolism in postmenopausal women: A randomized crossover trial.Obesity (Silver Spring, Md.) · 2023Trial
- The effect of morning vs evening exercise training on glycaemic control and serum metabolites in overweight/obese men: a randomised trial.Diabetologia · 2021Trial
- Exercise training elicits superior metabolic effects when performed in the afternoon compared to morning in metabolically compromised humans.Physiological reports · 2021Trial
- Four nights of sleep restriction suppress the postprandial lipemic response and decrease satiety.Journal of lipid research · 2019Trial
- Effects of Two-Week Sleep Extension on Glucose Metabolism in Chronically Sleep-Deprived Individuals.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2019Trial
- Acute sleep loss results in tissue-specific alterations in genome-wide DNA methylation state and metabolic fuel utilization in humans.Science advances · 2018Trial
- Skeletal muscle insulin signaling and whole-body glucose metabolism following acute sleep restriction in healthy males.Physiological reports · 2017Trial
- Trial
- Sex-specific circadian and behavioral phenotypes in aged growth hormone receptor knockout mice.GeroScience · 2026Article
- Mechanisms of Heat-Induced Sleep Disruption in Aging: A Narrative Review.Clocks & sleep · 2026Review
- Glucose homeostasis during recurrent periods of sleep restriction and recovery in healthy young adults.Sleep · 2026Article
- Circadian clock genes: Their influence on liver metabolism, disease development and treatment (Review).Molecular medicine reports · 2026Review
- Sleep duration inversely correlates with glucolipid metabolism in patients with new-onset type 2 diabetes mellitus.American journal of translational research · 2026Article
- Point Prevalence and Risk Factors for Insomnia in Children and Adolescents: Findings of a Population-Based Survey.Deutsches Arzteblatt international · 2025Observational
- Sleep Disruption and Atrial Fibrillation: Evidence, Mechanisms and Clinical Implications.Circulation research · 2025Review
- The Role of Sex in the Impact of Sleep Restriction on Appetite- and Weight-Regulating Hormones in Healthy Adults: A Systematic Review of Human Studies.Clocks & sleep · 2025Review
- Sleep habits in the pathogenesis and management of diabesity.Journal of diabetes investigation · 2025Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
contextShort sleep duration is associated with an increased risk of type 2 diabetes. Subchronic sleep restriction (SR) causes insulin resistance, but the mechanisms and roles of specific tissues are unclear.
objectiveThe purpose of this article was to determine whether subchronic SR altered (1) hepatic insulin sensitivity, (2) peripheral insulin sensitivity, and (3) substrate utilization.
designThis was a randomized crossover study in which 14 subjects underwent 2 admissions separated by a washout period. Each admission had 2 acclimatization nights followed by 5 nights of either SR (4 hours time in bed) or normal sleep (8 hours time in bed). MAIN OUTCOME MEASURE/
methodsInsulin sensitivity (measured by hyperinsulinemic-euglycemic clamp) and hepatic insulin sensitivity (measured by stable isotope techniques) were measured. In addition, we assayed stress hormone (24-hour urine free cortisol, metanephrine, and normetanephrine), nonesterified fatty acid (NEFA), and β-hydroxybutyrate (β-OH butyrate) levels. Resting energy expenditure (REE) and respiratory quotient (RQ) were measured by indirect calorimetry.
resultsCompared to normal sleep, whole-body insulin sensitivity decreased by 25% (P = .008) with SR and peripheral insulin sensitivity decreased by 29% (P = .003). Whereas hepatic insulin sensitivity (endogenous glucose production) did not change significantly, percent gluconeogenesis increased (P = .03). Stress hormones increased modestly (cortisol by 21%, P = .04; metanephrine by 8%, P = .014; normetanephrine by 18%, P = .002). Fasting NEFA and β-OH butyrate levels increased substantially (62% and 55%, respectively). REE did not change (P = 0.98), but RQ decreased (0.81 ± .02 vs 0.75 ± 0.02, P = .045).
conclusionSubchronic SR causes unique metabolic disturbances characterized by peripheral, but not hepatic, insulin resistance; this was associated with a robust increase in fasting NEFA levels (indicative of increased lipolysis), decreased RQ, and increased β-OH butyrate levels (indicative of whole-body and hepatic fat oxidation, respectively). We postulate that elevated NEFA levels are partially responsible for the decrease in peripheral sensitivity and modulation of hepatic metabolism (ie, increase in gluconeogenesis without increase in endogenous glucose production). Elevated cortisol and metanephrine levels may contribute to insulin resistance by increasing lipolysis and NEFA levels.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.