Background: Short sleep duration is a contributing factor for decreased insulin sensitivity and hyperglycemia. Sleep architecture represents a cyclical pattern of sleep that shifts between sleep Stages N1, N2, N3 (slow wave sleep) and Stage R (rapid eye movement sleep). The aim of the present study was to examine the association between sleep architecture and glucose and insulin metabolism in both normal weight and overweight/obese children and adolescents.
Methods: A total of 118 subjects participated in the study. Subjects under-went overnight polysomnography (PSG) when the percentage of total sleep time (% TST) spent at each sleep stage was recorded and an oral glucose tolerance test together was performed the next morning. We assessed glucose tolerance, insulin sensitivity and pancreatic β-cell function using 2-h glucose levels, the Matsuda index (IS(OGTT)), and insulin secretion-sensitivity index-2 (ISSI-2), respectively.
Results: After adjustment for age, gender, body mass index z-score, pubertal status, and obstructive apnea hypopnea index, Stage N3 (% TST) was positively associated with IS(OGTT), whereas Stage N1 (%TST) exerted an opposite effect on IS(OGTT). Higher sleep efficiency and longer TST were independently associated with lower 2-h glucose levels, higher ISSI-2 and/or higher IS(OGTT).
Conclusions: Stage N3, sleep efficiency and TST were protective factors in maintaining glucose and insulin homeostasis; however, Stage N1 functioned in the opposite direction.