Abstract

A majority of night shift workers have their circadian rhythms misaligned to their atypical schedule. While bright light exposure at night is known to reset the human central circadian clock, the behavior of peripheral clocks under conditions of shift work is more elusive. The aim of the present study was to quantify the resetting effects of bright light exposure on both central (plasma cortisol and melatonin) and peripheral clocks markers (clock gene expression in peripheral blood mononuclear cells, PBMCs) in subjects living at night. Eighteen healthy subjects were enrolled to either a control (dim light) or a bright light group. Blood was sampled at baseline and on the 4th day of simulated night shift. In response to a night-oriented schedule, the phase of PER1 and BMAL1 rhythms in PBMCs was delayed by ~2.5–3 h (P < 0.05), while no shift was observed for the other clock genes and the central markers. Three cycles of 8-h bright light induced significant phase delays (P < 0.05) of ~7–9 h for central and peripheral markers, except BMAL1 (advanced by +5h29; P < 0.05). Here, we demonstrate in humans a lack of peripheral clock adaptation under a night-oriented schedule and a rapid resetting effect of nocturnal bright light exposure on peripheral clocks.

Highlights

  • Shift work has been associated with a number of health consequences, such as increased risk of infection, obesity, diabetes, cardiovascular disorders, and cancer[1,2,3,4,5]

  • The circadian system comprises a central master clock located in the suprachiasmatic nucleus (SCN) of the hypothalamus and peripheral clocks found in most tissues and cell types[9,10]

  • For melatonin and cortisol rhythms, baseline phases and amplitudes were similar between control and bright light groups (P ≥ 0.93) and the phases occurred at conventional times-of-day: the melatonin levels peaked during the nocturnal sleep episode, whereas the peak of cortisol occurred shortly after lights on

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Summary

Introduction

Shift work has been associated with a number of health consequences, such as increased risk of infection, obesity, diabetes, cardiovascular disorders, and cancer[1,2,3,4,5]. Previous studies in humans showed that laboratory procedures such as simulated night shift or forced desynchrony (e.g. a 28-h day protocol) disrupt the circadian regulation of a number of physiological parameters such as leptin[6], glucose and insulin responses after meals[6], immune responses[7], and cardiovascular functions[8]. These alterations could contribute to the increased risk of medical conditions reported in shift workers such that interventions designed to alleviate circadian disturbances could have a preventive value.

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