Title: Disturbed glucoregulatory response to food intake after moderate sleep restriction. Author: Schmid SM, Hallschmid M, Jauch-Chara K, Wilms B, Lehnert H, Born J, Schultes B. Journal: Sleep; 2011 Mar 01; 34(3):371-7. PubMed ID: 21358855. Abstract: 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.[Abstract] [Full Text] [Related] [New Search]
