Our study aimed to assess the impact of one night of slow-wave sleep (SWS) suppression on glucose tolerance, and explore whether melatonin plays a role in glucose tolerance impairment after SWS suppression.
In sum, 20 volunteers participated in two experimental sessions: a session with SWS suppression during one night’s sleep and a session with a regular night’s sleep (control). Each session included collecting seven salivary samples. The following morning, an oral glucose tolerance test (OGTT) was performed.
SWS suppression effects depended on the individual blood glucose response to the OGTT. During the control session, ‘responders’ (N = 11), already presented with low glucose tolerance, which further declined after SWS suppression. ‘Non-responders’ (N = 9) experienced high glucose tolerance in both conditions. Among the responders, SWS suppression led to an increase in melatonin at the moment of awakening, while in non-responders melatonin increased during the first half of the night. In both conditions, responders were characterized by a shorter total sleep time (TST) and less rapid eye movement (REM) sleep. During SWS suppression, they had more non-rapid eye movement (NREM) stage 1 and longer nocturnal wakefulness. Responders and non-responders showed a comparable amount of SWS.
This study highlights three key findings: first, SWS suppression leads to an increase in salivary melatonin; second, melatonin’s effect on glucose tolerance depends on its secretion timing; and third, durations of REM sleep and nocturnal awakenings, appear to play an important role in melatonin secretion and glucose tolerance, indicating the potential clinical relevance of these findings for type 2 diabetes risk assessment.