Dim light at night disrupts molecular circadian rhythms and increases body weight.
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.
Department of Neuroscience and Institute for Behavioral Medicine Research, Wexner Medical Center, The Ohio State University, Columbus, OH 43210, USA. fonken.1@osu.edu
Laura K
LK
Fonken
Taryn G
TG
Aubrecht
O Hecmarie
OH
Meléndez-Fernández
Zachary M
ZM
Weil
Randy J
RJ
Nelson
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000502:physiology*; D056926:CLOCK Proteins / Q000096:biosynthesis / Q000235:genetics; D002940:Circadian Rhythm / Q000502:physiology*; D003345:Corticosterone / Q000378:metabolism; D005247:Feeding Behavior / Q000502:physiology; D007150:Immunohistochemistry; D008027:Light; D008029:Lighting; D008297:Male; D051379:Mice; D009043:Motor Activity; D016133:Polymerase Chain Reaction; D013493:Suprachiasmatic Nucleus / Q000378:metabolism / Q000502:physiology
D001786:Blood Glucose; D056926:CLOCK Proteins; D003345:Corticosterone
clock genes; feeding rhythm; light pollution; obesity