Cited by 156Sleep and Work-Related FatigueSleep and related disordersCircadian rhythm and melatonin

The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index; 1 of the 22 sources its claims cite were checked for support.

Sleep restriction increases free fatty acids in healthy men

Open access
Broussard, Josiane L., Chapotot, Florian, Abraham, Varghese, Day, Andrew, Delebecque, Fanny, Whitmore, Harry R., Tasali, Esra·2015·Diabetologia

Abstract

Aims/hypothesisSleep loss is associated with insulin resistance and an increased risk for type 2 diabetes, yet underlying mechanisms are not understood. Elevation of circulating non-esterified (i.e. free) fatty acid (NEFA) concentrations can lead to insulin resistance and plays a central role in the development of metabolic diseases. Circulating NEFA in healthy individuals shows a marked diurnal variation with maximum levels occurring at night, yet the impact of sleep loss on NEFA levels across the 24 h cycle remains unknown. We hypothesised that sleep restriction would alter hormones that are known to stimulate lipolysis and lead to an increase in NEFA levels.MethodsWe studied 19 healthy young men under controlled laboratory conditions with four consecutive nights of 8.5 h in bed (normal sleep) and 4.5 h in bed (sleep restriction) in randomised order. The 24 h blood profiles of NEFA, growth hormone (GH), noradrenaline (norepinephrine), cortisol, glucose and insulin were simultaneously assessed. Insulin sensitivity was estimated by a frequently sampled intravenous glucose tolerance test.ResultsSleep restriction relative to normal sleep resulted in increased NEFA levels during the nocturnal and early-morning hours. The elevation in NEFA was related to prolonged nocturnal GH secretion and higher early-morning noradrenaline levels. Insulin sensitivity was decreased after sleep restriction and the reduction in insulin sensitivity was correlated with the increase in nocturnal NEFA levels.Conclusions/interpretationSleep restriction in healthy men results in increased nocturnal and early-morning NEFA levels, which may partly contribute to insulin resistance and the elevated diabetes risk associated with sleep loss.

Overview

AI snapshot

Written from the paper’s full text.

TL;DR

In 19 healthy young men, four nights of sleep restriction (4.5 h in bed) increased nocturnal and early-morning non-esterified fatty acid (NEFA) levels and reduced insulin sensitivity compared with normal sleep (8.5 h in bed). The NEFA rise was linked to prolonged nocturnal growth hormone secretion and higher early-morning noradrenaline.

Key findings

  • Sleep restriction increased mean NEFA levels by approximately 15–30% during nocturnal and early-morning hours and prolonged the duration of the nocturnal NEFA increase by approximately 50 min.
  • Nocturnal GH secretion became biphasic in 14 of 19 participants and was prolonged by approximately 50 min; the increase in GH secretion duration correlated with prolonged NEFA rise (r = 0.81, p < 0.0001).
  • Early-morning noradrenaline increased by approximately 30% and correlated with the early-morning NEFA increase (r = 0.55, p = 0.015); evening/early-night cortisol was 23% higher but did not correlate with NEFA changes.
  • Insulin sensitivity by IVGTT decreased by 23% after sleep restriction (p = 0.004), and the decrease correlated with increased mean nocturnal NEFA (r = 0.52, p = 0.05) and nocturnal NEFA AUC (r = −0.53, p = 0.05); disposition index was lower (p = 0.042).

Methods

  • Randomised, controlled laboratory crossover study of 19 healthy young lean men aged 18–30 years, comparing four consecutive nights of 8.5 h in bed (normal sleep) versus 4.5 h in bed (sleep restriction), spaced at least 4 weeks apart.
  • 24 h blood profiles were collected at 15–30 min intervals for NEFA, GH, noradrenaline, cortisol, glucose and insulin; diet and energy intake were identical across conditions, and insulin sensitivity was estimated by frequently sampled IVGTT.
  • Analyses used mixed-model ANOVA with participants as random factor and sleep condition as fixed factor, Pearson correlations, and Benjamini–Hochberg correction for NEFA time-point comparisons; data reported as mean ± SEM.

Limitations

  • The paper states that it cannot exclude altered circadian timing as a contributor, provides no information on long-term effects of sleep restriction or recovery sleep, and notes that correlations do not demonstrate direct causality.
  • The paper notes the NEFA increase was modest (approximately 15–30%) and that future mechanistic studies, such as pharmacological NEFA suppression, are needed to test causality.
  • Evident from the text: the sample was small (n = 19) and restricted to healthy young lean men, limiting generalisability; technical difficulties invalidated IVGTT estimates in six normal-sleep and two sleep-restriction sessions, with five of the six normal-sleep invalid tests repeated.

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Integrity signals

Registry

Crossref · 10.1007/s00125-015-3500-4

Cites

36 of 36 references verified0 citation errors · 0 not checkable

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  • Probably not a substantial claim. 10
  • It may state two separate claims as one. 10
16 of 16
  • The paper relies on this without support.

    Growth hormone, noradrenaline and cortisol increase the rate of lipolysis and thereby raise circulating NEFA concentrations.

    “In addition, these hormones are known to increase the rate of lipolysis, resulting in elevated circulating NEFA concentrations.”
  • The paper relies on this without support.

    This study is the first to examine how sleep loss affects 24-hour NEFA profiles.

    “To our knowledge, this is the first study to examine the impact of sleep loss on 24 h NEFA profiles.”
2 of 2

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Metadata

Authors
Broussard, J. L., Chapotot, F., Abraham, V., Day, A., Delebecque, F., Whitmore, H. R., & Tasali, E.
Affiliations
  • Cedars-Sinai Medical Center (US)
  • University of Chicago (US)
  • University of Wisconsin–Madison (US)
Corresponding author
Broussard, Josiane L.
Venue
Diabetologia
Published
2015-02-22
Volume
58
Issue
4
Pages
791-798
ISSN
  • 0012-186X (ISSN-L)
  • 1432-0428
OpenAlex
W2009304756
Cited by
156
References
36
Citations by year
2026: 9 · 2025: 17 · 2024: 12 · 2023: 7 · 2022: 19 · 2021: 15 · 2020: 8 · 2019: 14 · 2018: 22 · 2017: 15 · 2016: 9 · 2015: 9
FWCI
27.61
Type
journal article
Language
en
Open access
Locations
  • Diabetologia (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • U.S. Department of Defense (W81XWH)
  • University of Chicago (UL1 TR000430)
  • Georgia Clinical and Translational Science Alliance (UL1 TR000430)
  • National Institutes of Health (UL1TR000430, W81XWH, P60 DK20595, TR000430)
  • National Institute on Aging (P01-AG11412., P01AG011412)
  • National Heart, Lung, and Blood Institute (R01HL086459, R01HL075079, T32HL007909)
  • National Institute of Diabetes and Digestive and Kidney Diseases (P60DK20595, P60DK020595, P30DK020595)
  • National Center for Research Resources (P41RR013642)
  • National Center for Advancing Translational Sciences (CTSA-UL1 TR000430)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (P50HD057796)
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, free fatty acids, insulin resistance, type 2 diabetes risk, growth hormone, norepinephrine, cortisol, lipolysis, insulin sensitivity, circadian rhythm
MeSH terms
Adolescent, Adult, Blood Glucose, Circadian Rhythm, Fatty Acids, Nonesterified, Humans, Hydrocortisone, Insulin, Insulin Resistance, Male, Norepinephrine, Random Allocation, Sleep, Sleep Deprivation, Time Factors, Biomarkers, Up-Regulation, Human Growth Hormone, Young Adult, Healthy Volunteers

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