Abstract
Objectives: Experimentally induced sleep dysfunction has been consistently linked with ghrelin dysregulation, which may play a role in T2D pathophysiology. This study examined whether a) one-week, at-home, objective measures of sleep duration and sleep duration variability were associated with pre- and post-prandial ghrelin regulation throughout the day; and b) whether these relationships were moderated by insulin sensitivity and meal administration time.
Methods: The study assessed 103 adults (72% men, 18-55 years) with no diagnosed conditions. Measures included insulin sensitivity via hyperinsulinemia clamp, sleep function using at-home actigraphy data over one week, and ghrelin via blood samples collected across two in-patient laboratory days, wherein 4 meals per day were provided. Participants received, in randomized order, a standard U.S. caloric load on one day and a high caloric load on the other. Hierarchical linear modeling examined whether the interactions among sleep measures (duration and variability), insulin sensitivity, and meal administration time were associated with pre- and post-prandial ghrelin levels on the standard and high calorie days.
Results: No significant effects of sleep duration were found. However, with lower insulin sensitivity, elevated sleep variability was associated with higher pre- and post-prandial ghrelin levels, and with greater net incremental post-prandial ghrelin suppression on both caloric load days (meals 1 – 4). In contrast, with higher insulin sensitivity, elevated sleep variability was not associated with pre-prandial ghrelin levels, but was associated with lower post-prandial ghrelin levels and greater net incremental post-prandial ghrelin suppression at the evening meal (meal 4).
Conclusions: The study revealed novel linkages of habitual sleep variability with ghrelin regulation that differed by extent of insulin sensitivity and meal administration time. Further research is needed to examine whether these associations continue to be altered as a function of T2D progression.