Background: Human sleep is composed of different sleep stages, of which slow wave sleep (SWS) is an important modulator of glucose regulation. Curtailment of sleep duration in general and of slow wave sleep (SWS) in particular reduces glucose tolerance in healthy subjects. Previously, we have reported that a single night of partial sleep deprivation reduces insulin sensitivity by 1520% in patients with type 1 diabetes. We hypothesized that this effect could be a consequence of reduced SWS.
Objective: To determine the effect of selective suppression of SWS on insulin sensitivity in patients with type 1 diabetes.
Methods: We studied insulin sensitivity in seven patients with type 1 diabetes on continuous s.c. insulin infusion therapy without any known sleep disorders after a normal night of sleep and after a night of suppressed SWS. Objective sleep parameters were determined by polysomnography. SWS was suppressed by delivering acoustic tones of varying frequency, to replace SWS with shallow sleep without awakening the patients. The following morning, glucose metabolism was studied by hyperinsulinemic euglycemic clamp studies with infusion of (6.6-2H2) glucose.
Results: The amount of SWS was suppressed by 75% (P<0.001) without a reduction in total sleep duration (471 vs 480 min, P=0.63). SWS suppression did not affect endogenous glucose production in the basal state nor during clamp conditions compared to normal sleep. During clamp conditions, SWS suppression did not result in differences in glucose infusion rates (22.6±3.1vs 22.3±3.2 μmol/kg LBM-1 per min, P=0.95) or glucose disposal rate (31.6±2.9 vs 30.0±2.7 μmol/kg LBM-1 per min, P=0.65). SWS suppression did not affect plasma free fatty acid levels.
Conclusions: Selective suppression of SWS sleep during a single night does not influence insulin sensitivity in patients with type 1 diabetes. Therefore, the reduction in insulin sensitivity by partial sleep deprivation can not be explained by a reduced amount of SWS.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.
05 - 09 May 2012
European Society of Endocrinology