Effect of acute sleep restriction on the concentration of serum soluble leptin receptor in healthy adult females

Abstract

Sleep restriction is now considered to be a worldwide epidemic, as over 20% of people around the world are sleep deprived. Although sleep deprivation is now an overlooked feature of modern societies, it entails considerable adverse effects on physiological systems, one being energy homeostasis. A corpus of research has demonstrated that leptin, a key hormone that conveys the body's energy status to the brain, decreases after sleep restriction, which may partly account for the associated alteration in body metabolism; however little information is available regarding the underlying physiological mechanisms. The aim of the present study was to investigate the diurnal serum profile of both leptin and its soluble receptor- sOB-R- before and after acute sleep restriction. Five healthy adult females (20-30 years old; BMI 22-26) were maintained on an 8-hour sleep/wake schedule (bedtime at 12:00 AM) for one week [baseline or control (C) period]. This was followed by 2 consecutive nights of a 4.5-hour nocturnal sleep opportunity [sleep restriction (SR), bedtime at 3:30AM]. Throughout the duration of the study, sleep parameters were objectively measured using wrist actigraphy and participants were asked to keep a food and sleep diary. For the determination of circulating free hormone and soluble receptor levels, blood and saliva samples were collected from 'each subject at 4-hour intervals (starting 8:00AM) on the days before and following SR. Results showed that the diurnal serum levels of free leptin and sOB-R were out-of-phase (discordant) with respect to each other before and following SR. Leptin levels were significantly elevated in the early morning, mid-afternoon, and midnight; while sOB-R levels were high around noontime and late evening. SR did not affect the diurnal serum pattern of both free hormone and its receptor, but rather altered their average daily concentrations. That is, SR caused a significant decrease in circulating free leptin levels (SR, 20.94 ± 1.71 ng/ml vs. C, 25.71 ± 1.71 ng/ml; P < 0.01) and a concomitant increase in sOB-R levels relative to baseline (SR, 24.39 ± 1.21 ng/ml vs. C, 19.79± 1.643 ng/ml; P <0.01). These findings may suggest that SR works on modulating circulating free leptin levels, and thus its regulatory role on body metabolism (or energy homeostasis), via regulating sOB-R levels. The putative regulatory role of leptin on its soluble receptor may have valuable implications on therapeutic approaches that may consider sOB-R as a potential target for countering body weight disorders and metabolic disturbances associated with disturbed sleep.