Abstract
The influence of sleep duration on metabolic pathogenic pathways associated with Type 2 diabetes mellitus are not well understood but may be operational long before the development of clinical diabetes or even prediabetes is detected. This study was designed to examine in preclinical nondiabetic adults whether the association of insulin sensitivity and postprandial metabolic function is moderated by sleep duration. The sample was comprised of 143 individuals (65% men), aged 18–55 years, who had no diabetes or other diagnosed conditions. Metabolic function outcomes were assessed in response to an OGTT, and two 14-h serial mixed carbohydrate-meal tests 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). Sleep duration over 1-week was derived using actigraphy. Quantitative modeling was applied to derive total postprandial insulinemia (AUCINS), total postprandial glycemia (AUCGLU), β-cell glucose sensitivity (β-GS), early insulin secretion rate sensitivity (ESRS), and potentiation ratio (POT). Study findings indicated that the relationship between insulin sensitivity and postprandial insulin response following a carbohydrate load depended on sleep duration, even after controlling for relevant covariates. Specifically, with more insulin resistance and shorter sleep duration, more elevated postprandial insulin secretion was observed to the double carbohydrate load condition. These findings reflect a compensatory adaptation of postprandial insulin metabolism in insulin resistance that is heightened with shorter sleep duration. Although there was no moderation of the association of insulin sensitivity with AUCGLU and ESRS by sleep duration, moderation was observed for β-GS and POT. However, the pattern of these relationships suggest that these metabolic parameters do not account for the moderation of the association of insulin sensitivity and postprandial insulinemia by sleep duration. Thus, some mechanism other than that measured in this study is responsible for the differences in insulin metabolic response to high carbohydrate loading in these individuals. Further studies are necessary to delineate whether there are alterations in some aspect of sleep function or architecture beyond sleep duration that may mediate the heightened insulin secretion response to high carbohydrate loading in insulin resistant individuals.