A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects.
Level 3 - non-randomized controlled study
Non-randomized controlled crossover physiological trial in healthy humans
PubMed 20371664 · doi:10.1210/jc.2009-2430
What was done
Nine healthy subjects (5 men, 4 women) were studied after a night of normal sleep (2300 to 0730 h) and after a night of 4 hours of sleep (0100 to 0500 h). Sleep was measured by polysomnography. Insulin sensitivity and endogenous glucose production were evaluated the following day using hyperinsulinemic euglycemic clamp studies (1130 to 1430 h) with [6,6-2H2]glucose tracer infusion.
What was found
Sleep duration was shorter during the restricted night compared to normal sleep (226 +/- 11 vs. 454 +/- 9 min, P < 0.0001). Basal levels of glucose, nonesterified fatty acids, insulin, and endogenous glucose production were not altered. During the clamp, sleep restriction increased endogenous glucose production (4.4 +/- 0.3 vs. 3.6 +/- 0.2 micromol x kg lean body mass^-1 x min^-1, P = 0.017), decreased glucose disposal rate (32.5 +/- 3.6 vs. 40.7 +/- 5.1 micromol x kg lean body mass^-1 x min^-1, P = 0.009), decreased glucose infusion rate by approximately 25% (P = 0.001), and increased plasma nonesterified fatty acid levels (68 +/- 5 vs. 57 +/- 4 micromol/liter, P = 0.005).
Why it matters
A single night of short sleep acutely induces insulin resistance across hepatic, peripheral, and adipose tissue pathways in healthy humans.
Limits
The study had a very small sample size of 9 healthy individuals. The abstract does not state whether condition order was randomized or specify the washout interval between test nights, and clinical outcomes in diabetic populations were not directly measured.
Cited by
- supports A single night of sleep deprivation, or two to three nights of sleep deprivation, causes acute insulin resistance and elevated inflammation.