Abstract: With the exception of high latitudes, life has evolved under bright days and dark nights. Most organisms have developed endogenously driven circadian rhythms that are synchronized to this daily light/dark cycle. In recent years, humans have shifted away from the naturally occurring solar light cycle in favor of artificial and sometimes irregular light schedules produced by electric lighting. Exposure to unnatural light cycles is increasingly associated with obesity and metabolic syndrome; however, the means by which environmental lighting alters metabolism are poorly understood. Thus, we exposed mice to dim light at night and investigated changes in the circadian system and metabolism. Here we report that exposure to ecologically relevant levels of dim (5 lux) light at night altered core circadian clock rhythms in the hypothalamus at both the gene and protein level. Circadian rhythms in clock expression persisted during light at night; however, the amplitude of Per1 and Per2 rhythms was attenuated in the hypothalamus. Circadian oscillations were also altered in peripheral tissues critical for metabolic regulation. Exposure to dimly illuminated, as compared to dark, nights decreased the rhythmic expression in all but one of the core circadian clock genes assessed in the liver. Additionally, mice exposed to dim light at night attenuated Rev-Erb expression in the liver and adipose tissue. Changes in the circadian clock were associated with temporal alterations in feeding behavior and increased weight gain. These results are significant because they provide evidence that mild changes in environmental lighting can alter circadian and metabolic function. Detailed analysis of temporal changes induced by nighttime light exposure may provide insight into the onset and progression of obesity and metabolic syndrome, as well as other disorders involving sleep and circadian rhythm disruption.

Abstract: Artificial moonlight was recently shown to shift the endogenous clock of fruit flies and make them nocturnal. To test whether this nocturnal activity is partly due to masking effects of light, we exposed the clock-mutants per(01), tim(01), per(01);tim(01), cyc(01), and Clk(JRK) to light/dark and light/dim-light cycles and determined the activity level during the day and night. We found that under moonlit nights, all clock mutants shifted their activity significantly into the night, suggesting that this effect is independent of the clock. We also recorded the flies under continuous artificial moonlight and darkness to judge the effect of dim constant light on the activity level. All mutants, except Clk(JRK) flies, were significantly more active under artificial moonlight conditions than under complete darkness. Unexpectedly, we found residual rhythmicity of per(01) and especially tim(01) mutants under these conditions, suggesting that TIM and especially PER retained some activity in the absence of its respective partner. Nevertheless, as even the double mutants and the cyc(01) and Clk(JRK) mutants shifted their activity into the night, we conclude that dim light stimulates the activity of fruit flies in a clock-independent manner. Thus, nocturnal light has a twofold influence on flies: it shifts the circadian clock, and it increases nocturnal activity independently of the clock. The latter was also observed in some primates by others and might therefore be of a more general validity.