Sleeping oxygen saturation, rapid eye movement sleep, and the adaptation of postprandial metabolic function in insulin sensitive and resistant individuals without diabetes
Sleeping oxygen saturation (SaO2) and sleep stage duration have been linked with prediabetic alterations but the pathogenic pathways are not well understood. This study of insulin sensitive and resistant adults examined the effect on postprandial metabolic regulation of repeated mixed-meal challenges of different carbohydrate loading. The aim was to examine whether the relationship between lower sleeping oxygen saturation (SaO2) and poorer fasting and postprandial metabolic function may be linked with reduced slow wave sleep (SWS) and rapid eye movement (REM) duration, independent of age, sex and total adiposity.
The 24 men and women, aged 25-54 years, had no diabetes or other diagnosed conditions, were evaluated with polysomnography to derive indices of SaO2 and sleep architecture. In addition, an OGTT and two 14-h serial mixed-meal tests were administered over 3 successive in-patient days. The carbohydrate content of the mixed-meals was manipulated to compare a standard-load day with a double-load day (300 vs. 600 kcal/meal). Quantitative modeling was applied to derive β-cell glucose sensitivity (β-GS), early insulin secretion rate sensitivity (ESRS), and total postprandial insulinemia (AUCINS).
Analyses showed that, for the 14-h tests, the SaO2 relationship with metabolic outcomes was associated significantly with percent time spent in REM but not SWS, independent of age, sex and total adiposity. Specifically, indirect pathways indicated that lower SaO2 was related to shorter REM duration, and shorter REM was respectively associated with higher β-GS, ESRS, and AUCINS for the 300- and 600-load days (300 kcal/meal: β = -8.68, p < .03, β = -8.54, p < .002, and β = -10.06, p < .008; 600 kcal/meal: β = -11.45, p < .003, β = -11.44, p < .001, and β = -11.00, p < .03).
Sleeping oxygen desaturation and diminished REM duration are associated with a metabolic pattern that reflects a compensatory adaptation of postprandial insulin metabolism accompanying preclinical diabetic risk.
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