Abstract
Exposure to light at night has been steadily increasing since industrialization. Light at night comes from light bulbs, light pollution produced by cities, and more recently from the widespread use of personal electronics (smart phones, tablets, laptops) at night. Previous studies in outbred mice have shown that dim light at night (DLAN) disrupts circadian rhythms and increases body weight, but it is unknown whether DLAN affects the development of cardiovascular disease. In this project, we are testing the hypothesis that DLAN accelerates the development of atherosclerotic lesions in C57BL/6J Apolipoprotein E‐deficient (ApoE−/−) mice. We single‐housed male ApoE−/− mice in light‐tight boxes at 7 weeks of age for 1 week in 12h light:12h dark (12L:12D) and then in DLAN (12h light: 12h dim 5 lux light) for 12 weeks. Control mice were maintained in 12L:12D for 13 weeks. Body weights did not differ between ApoE−/− mice in 12L:12D and DLAN. In 12L:12D, ApoE−/− mice had a robust daily rhythm of eating behavior that peaked during the night. However, after a few days in DLAN, ApoE−/− mice had a low‐amplitude eating behavior rhythm that persisted for the entire experiment. Preliminary data also suggest that ApoE−/− mice in DLAN had increased atherosclerotic lesion area and serum cholesterol levels compared to ApoE−/− mice in 12L:12D. These data suggest that DLAN disrupts the daily rhythm of eating behavior and may also increase atherosclerosis.Support or Funding InformationThis research was supported by the National Institutes of Health awards P20GM103527 and R03DK107851, an American Physiological Society Undergraduate Summer Research Fellowship, and the University of Kentucky. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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