Study objectives: Epidemiological studies point to a strong association between short sleep duration and the development of diabetes. We examined the hypothesis that short-term sleep loss decreases glucose tolerance and insulin sensitivity and, if so, how these changes relate to hypothalamic-pituitary-adrenal (HPA) secretory activity and markers of subclinical inflammation.
Design: In a balanced, within-subject design, circulating glucose, insulin, C-peptide, glucagon, ACTH, cortisol, and IL-6 levels were closely monitored during a 15-h daytime period following 2 nights of restricted sleep (02:45-07:00) and 2 nights of regular sleep (bedtime 22:45-07:00), respectively.
Setting: Time-deprivation suite within a university medical center sleep laboratory.
Participants: 15 healthy, unmedicated normal-weight men.
Intervention: Sleep restriction.
Measurements and results: Pre-breakfast concentrations of blood parameters were unchanged following sleep manipulation (P > 0.30). However, insulin and glucose peak responses to breakfast intake at 08:00 were distinctly increased by sleep restriction in comparison to regular sleep (398.5 ± 57.4 vs. 284.3 ± 51.5 pmol/L and 6.8 ± 0.3 vs. 6.1 ± 0.3 mmol/L, respectively; all P < 0.02), while glucagon responses were blunted by sleep loss (P = 0.03). There were no differences in circulating ACTH, cortisol, and IL-6 concentrations between the 2 conditions (all P > 0.25).
Conclusions: Data indicate an impairment of glucose tolerance after 2 days of sleep restriction to ~4 h that appears to be primarily caused by a reduction in insulin sensitivity. Unchanged HPA secretory activity and IL-6 concentrations argue against a mediation of these effects by stress-related or inflammatory mechanisms.
Keywords: Sleep deprivation; glucagon; glucose tolerance; insulin resistance; insulin sensitivity.