Slow-wave sleep and the risk of type 2 diabetes in humans

Abstract

There is convincing evidence that, in humans, discrete sleep stages are important for daytime brain function, but whether any particular sleep stage has functional significance for the rest of the body is not known. Deep non-rapid eye movement (NREM) sleep, also known as slow-wave sleep (SWS), is thought to be the most "restorative" sleep stage, but beneficial effects of SWS for physical well being have not been demonstrated. The initiation of SWS coincides with hormonal changes that affect glucose regulation, suggesting that SWS may be important for normal glucose tolerance. If this were so, selective suppression of SWS should adversely affect glucose homeostasis and increase the risk of type 2 diabetes. Here we show that, in young healthy adults, all-night selective suppression of SWS, without any change in total sleep time, results in marked decreases in insulin sensitivity without adequate compensatory increase in insulin release, leading to reduced glucose tolerance and increased diabetes risk. SWS suppression reduced delta spectral power, the dominant EEG frequency range in SWS, and left other EEG frequency bands unchanged. Importantly, the magnitude of the decrease in insulin sensitivity was strongly correlated with the magnitude of the reduction in SWS. These findings demonstrate a clear role for SWS in the maintenance of normal glucose homeostasis. Furthermore, our data suggest that reduced sleep quality with low levels of SWS, as occurs in aging and in many obese individuals, may contribute to increase the risk of type 2 diabetes.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Fig. 1.

S.I., AIRg, DI, and glucose tolerance at baseline and after 3 nights of SWS suppression. The data are means ± SEM (n = 9 subjects). The asterisks indicate significant differences (paired t test): S.I. (P = 0.009) (a); AIRg (P = 0.73) (b); DI (P = 0.02) (c); and glucose tolerance (P = 0.03) (d).

Fig. 2.

Relationships between the changes in SWS and changes in S.I. and acute insulin response to glucose. (a) SWS at baseline and SWS after intervention (r = 0.81, P = 0.009). (b) SWS at baseline and decrease in SWS after 3 nights of SWS suppression (r = 0.97, P = 0.0001). (c) Decrease in SWS and change in S.I. after 3 nights of SWS suppression (r = 0.89, P = 0.001). (d) Decrease in SWS and change in AIRg after 3 nights of SWS suppression (r = 0.70, P = 0.03).

Fig. 3.

Sleep architecture during SWS suppression on night 1 (N1), night 2 (N2), and night 3 (N3) vs. the baseline night (B1). The data are means ± SEM (n = 9 subjects). The asterisks indicate significant differences (ANOVA): total sleep time (P = 0.14 for N1, N2, and N3 vs. baseline) (a); REM sleep (P = 0.29 for N1, N2, and N3 vs. baseline) (b); SWS (P = 0.0001 for N1, N2, and N3 vs. baseline) (c); stage 2 of NREM sleep (P = 0.0001 for N1, N2, and N3 vs. baseline) (d); wake time (P = 0.12 for N1, N2, and N3 vs. baseline) (e); and total microarousal index (P = 0.0002 for N1, N2, and N3 vs. baseline) (f).

Fig. 4.

Profiles of delta power (μV2) for the first four NREM–REM sleep cycles (NREM1, NREM2, NREM3, and NREM4). The data are means ± SEM. (a) Baseline night (B1). (b) First night of SWS suppression (N1). (c) Second night of SWS suppression (N2). (d) Third night of SWS suppression (N3). In all experimental nights, as compared with baseline, the amount of delta power was reduced by ≈44–48% for NREM1 (P < 0.002, ANOVA), by ≈50–55% for NREM2 (P < 0.001, ANOVA), by ≈16–30% for NREM3 (P, not significant), and by ≈8–17% for NREM4 (P, not significant).