Impaired insulin signaling in human adipocytes after experimental sleep restriction: a randomized, crossover study.
Level 2 - randomized trial
Randomized crossover trial
PubMed 23070488 · doi:10.7326/0003-4819-157-8-201210160-00005
What was done
Seven healthy adults (1 woman, 6 men; mean age 23.7 years, mean BMI 22.8 kg/m2) participated in a randomized, two-period crossover study conducted in a clinical research center. Participants underwent 4 days of sleep restriction (4.5 hours in bed per night) and 4 days of normal sleep (8.5 hours in bed per night) under controlled caloric intake and physical activity. Following each condition, subcutaneous fat biopsies were collected, and adipocytes were tested for insulin-stimulated Akt phosphorylation (pAkt/tAkt ratio). Total body insulin sensitivity was evaluated using a frequently sampled intravenous glucose tolerance test.
What was found
The insulin concentration required for half-maximal pAkt-tAkt stimulation in adipocytes was nearly threefold higher after sleep restriction than after normal sleep (mean 0.71 nM [SD, 0.27] vs. 0.24 nM [SD, 0.24]; P = 0.01; mean difference 0.47 nM [SD, 0.33]; P = 0.01). The total area under the receiver-operating characteristic curve for the pAkt-tAkt response decreased by 30% during sleep restriction (P = 0.01). Total body insulin sensitivity was also significantly reduced (P = 0.02).
Why it matters
This study provides direct experimental evidence that short-term sleep restriction impairs insulin signaling at the cellular level in human peripheral adipose tissue, linking poor sleep directly to peripheral metabolic dysfunction.
Limits
The sample size was extremely small (n = 7) and recruited from a single center. The cohort was young, lean, and predominantly male, limiting generalizability to older, overweight, or clinically diverse populations. The study evaluated only 4 days of sleep restriction, leaving the long-term persistence and reversibility of these cellular changes unexamined.
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