Interactive effects of light at night and high fructose intake on the central circadian clock and endocrine outputs in rats

Light pollution is an increasing global environmental risk factor that contributes to the recent burden of metabolic diseases. The underlying mechanisms are not understood, but disruption of circadian control of physiological and behavioural processes may be involved. The negative consequences of chronodisruption can be augmented by co-exposure to high energy intake. Therefore, we investigated the individual and combined effects of artificial light at night (ALAN) and 10 % fructose in drinking water on the central clock in the suprachiasmatic nuclei (SCN) of the hypothalamus and circadian hormonal outputs in male rats. After 10 weeks of ALAN exposure and high fructose intake, the clockwork in the SCN was attenuated as indicated by eliminated day/night differences in the core clock gene Per1. Additionally, ALAN suppressed the daily variability and fructose induced upregulation of a gamma-aminobutyric acid-synthesising enzyme (GAD65), potentially affecting inhibitory neurotransmission in the SCN. ALAN and fructose additively inhibited plasma melatonin levels revealing excessive fructose intake as a chronodisruptive factor that can be potentiated by ALAN. In contrast to melatonin, daytime plasma testosterone concentrations were increased by high fructose and supressed by ALAN. Furthermore, high fructose intake elevated the plasma levels of two adipokines, leptin and adiponectin, but this response was absent specifically during the daytime in rats exposed to ALAN, indicating that ALAN reduced adipose tissue responsiveness. Our results document the complex consequences of ALAN and high fructose intake on endocrine control mechanisms that can have a long-term negative impact on metabolic health.