Abstract

Appropriately timed light is critical for circadian organization; exposure to dim light at night (dLAN) disrupts temporal organization of endogenous biological timing. Exposure to dLAN in adult mice is associated with elevated body mass and changes in metabolism putatively driven by voluntary changes in the time of food intake. We predicted that exposure of young mice to LAN could affect adult metabolic function. At 3 weeks (Experiment 1) or 5 weeks (Experiment 2) of age, mice were either maintained in standard light-dark (DARK) cycles or exposed to nightly dLAN (5 lux). In the first two experiments, food intake and locomotor activity were assessed after 4 weeks and a glucose tolerance test was administered after 6 weeks in experimental lighting conditions. In Experiment 3, tissues were collected around the clock at 6 h intervals to investigate rhythmic hepatic clock gene expression in mice exposed to dLAN from 3 or 5 weeks of age. Male and female mice exposed to dLAN beginning at 3 weeks of age displayed similar growth rates and body mass to DARK-reared offspring, despite increasing day-time food intake. Exposure to dLAN beginning at 5 weeks of age increased body mass and daytime food intake in male, but not female, mice. Consistent with the body mass phenotype, clock gene expression was unaltered in the liver. In contrast to adults, dLAN exposure during the development of the peripheral circadian system has sex- and development-dependent effects on body mass gain.

Highlights

  • Postnatal life is a critical time for shaping both neural and physiological systems, influencing physiology, behavior, and health in adulthood (Plagemann et al, 2012)

  • Somatic Measures When exposed to dim light at night (dLAN) starting at 3 weeks of age, neither males (Figure 1A) nor females (Figure 1B) gained body mass relative to mice housed in dark nights (p > 0.05)

  • Food Intake Mice exposed to dLAN ate more during the daytime than mice exposed to DARK nights [F(1, 33) = 7.74, p < 0.01; Figure 1D]

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Summary

Introduction

Postnatal life is a critical time for shaping both neural and physiological systems, influencing physiology, behavior, and health in adulthood (Plagemann et al, 2012). Social and physiological stressors during gestation and early postnatal development have long–term effects into adulthood (Fagundes et al, 2013; Szyf, 2013). Life is a critical time for shaping the circadian system (Davis and Reppert, 2001). Circadian rhythms are endogenous 24-h cycles of physiology and behavior, synchronized to the external day-night cycle by photic input to the suprachiasmatic nucleus (SCN) of the hypothalamus. Endogenous rhythmicity is maintained by a transcriptional-translational feedback loop consisting of a core set of clock genes (Mohawk et al, 2012). Rhythmic clock gene expression in the rodent SCN is solidified and responsive to

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