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Author (down) Gooley, J.J.; Chamberlain, K.; Smith, K.A.; Khalsa, S.B.S.; Rajaratnam, S.M.W.; Van Reen, E.; Zeitzer, J.M.; Czeisler, C.A.; Lockley, S.W. url  doi
openurl 
  Title Exposure to room light before bedtime suppresses melatonin onset and shortens melatonin duration in humans Type Journal Article
  Year 2011 Publication The Journal of Clinical Endocrinology and Metabolism Abbreviated Journal J Clin Endocrinol Metab  
  Volume 96 Issue 3 Pages E463-72  
  Keywords Adolescent; Adult; Female; Humans; *Light; *Lighting; Male; Melatonin/*blood; Sleep/physiology; Time Factors; Young Adult  
  Abstract CONTEXT: Millions of individuals habitually expose themselves to room light in the hours before bedtime, yet the effects of this behavior on melatonin signaling are not well recognized. OBJECTIVE: We tested the hypothesis that exposure to room light in the late evening suppresses the onset of melatonin synthesis and shortens the duration of melatonin production. DESIGN: In a retrospective analysis, we compared daily melatonin profiles in individuals living in room light (<200 lux) vs. dim light (<3 lux). PATIENTS: Healthy volunteers (n = 116, 18-30 yr) were recruited from the general population to participate in one of two studies. SETTING: Participants lived in a General Clinical Research Center for at least five consecutive days. INTERVENTION: Individuals were exposed to room light or dim light in the 8 h preceding bedtime. OUTCOME MEASURES: Melatonin duration, onset and offset, suppression, and phase angle of entrainment were determined. RESULTS: Compared with dim light, exposure to room light before bedtime suppressed melatonin, resulting in a later melatonin onset in 99.0% of individuals and shortening melatonin duration by about 90 min. Also, exposure to room light during the usual hours of sleep suppressed melatonin by greater than 50% in most (85%) trials. CONCLUSIONS: These findings indicate that room light exerts a profound suppressive effect on melatonin levels and shortens the body's internal representation of night duration. Hence, chronically exposing oneself to electrical lighting in the late evening disrupts melatonin signaling and could therefore potentially impact sleep, thermoregulation, blood pressure, and glucose homeostasis.  
  Address Division of Sleep Medicine, Brigham and Women's Hospital and Harvard Medical School, 221 Longwood Avenue, Boston, Massachusetts 02115, USA. gmsjjg@nus.edu  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0021-972X ISBN Medium  
  Area Expedition Conference  
  Notes PMID:21193540; PMCID:PMC3047226 Approved no  
  Call Number IDA @ john @ Serial 139  
Permanent link to this record
 

 
Author (down) Fonken, L.K.; Lieberman, R.A.; Weil, Z.M.; Nelson, R.J. url  doi
openurl 
  Title Dim light at night exaggerates weight gain and inflammation associated with a high-fat diet in male mice Type Journal Article
  Year 2013 Publication Endocrinology Abbreviated Journal Endocrinology  
  Volume 154 Issue 10 Pages 3817-3825  
  Keywords Adipose Tissue, White/*immunology/metabolism/pathology; Animals; Antigens, CD11b/biosynthesis/genetics/metabolism; Appetite Regulation/*radiation effects; Arcuate Nucleus/*immunology/metabolism/pathology; Behavior, Animal/radiation effects; Circadian Rhythm; Cytokines/biosynthesis/genetics/metabolism; Diet, High-Fat/*adverse effects; Feeding Behavior/radiation effects; Gene Expression Regulation; Glucose Intolerance/etiology/immunology/metabolism/pathology; I-kappa B Kinase/biosynthesis/genetics/metabolism; Insulin Resistance; Lighting/*adverse effects; Male; Mice; Microglia/immunology/metabolism/pathology; Nerve Tissue Proteins/biosynthesis/genetics/metabolism; Obesity/*etiology/immunology/metabolism/pathology; Random Allocation; *Weight Gain  
  Abstract Elevated nighttime light exposure is associated with symptoms of metabolic syndrome. In industrialized societies, high-fat diet (HFD) and exposure to light at night (LAN) often cooccur and may contribute to the increasing obesity epidemic. Thus, we hypothesized that dim LAN (dLAN) would provoke additional and sustained body mass gain in mice on a HFD. Male mice were housed in either a standard light/dark cycle or dLAN and fed either chow or HFD. Exposure to dLAN and HFD increase weight gain, reduce glucose tolerance, and alter insulin secretion as compared with light/dark cycle and chow, respectively. The effects of dLAN and HFD appear additive, because mice exposed to dLAN that were fed HFD display the greatest increases in body mass. Exposure to both dLAN and HFD also change the timing of food intake and increase TNFalpha and MAC1 gene expression in white adipose tissue after 4 experimental weeks. Changes in MAC1 gene expression occur more rapidly due to HFD as compared with dLAN; after 5 days of experimental conditions, mice fed HFD already increase MAC1 gene expression in white adipose tissue. HFD also elevates microglia activation in the arcuate nucleus of the hypothalamus and hypothalamic TNFalpha, IL-6, and Ikbkb gene expression. Microglia activation is increased by dLAN, but only among chow-fed mice and dLAN does not affect inflammatory gene expression. These results suggest that dLAN exaggerates weight gain and peripheral inflammation associated with HFD.  
  Address Department of Neuroscience, Wexner Medical Center, The Ohio State University, 636 Biomedical Research Tower, 460 West 12th Avenue, Columbus, Ohio 43210. fonken.1@osu.edu  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0013-7227 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23861373 Approved no  
  Call Number IDA @ john @ Serial 93  
Permanent link to this record
 

 
Author (down) Figueiro, M.G.; Rea, M.S. url  doi
openurl 
  Title The effects of red and blue lights on circadian variations in cortisol, alpha amylase, and melatonin Type Journal Article
  Year 2010 Publication International Journal of Endocrinology Abbreviated Journal Int J Endocrinol  
  Volume 2010 Issue Pages 829351  
  Keywords blue light; red light; circadian rhythm; cortisol; alpha amylase; melatonin; photobiology; suprachiasmatic nuclei; endocrinology  
  Abstract The primary purpose of the present study was to expand our understanding of the impact of light exposures on the endocrine and autonomic systems as measured by acute cortisol, alpha amylase, and melatonin responses. We utilized exposures from narrowband long-wavelength (red) and from narrow-band short-wavelength (blue) lights to more precisely understand the role of the suprachiasmatic nuclei (SCN) in these responses. In a within-subjects experimental design, twelve subjects periodically received one-hour corneal exposures of 40 lux from the blue or from the red lights while continuously awake for 27 hours. Results showed-that, as expected, only the blue light reduced nocturnal melatonin. In contrast, both blue and red lights affected cortisol levels and, although less clear, alpha amylase levels as well. The present data bring into question whether the nonvisual pathway mediating nocturnal melatonin suppression is the same as that mediating other responses to light exhibited by the endocrine and the autonomic nervous systems.  
  Address Lighting Research Center, Rensselaer Polytechnic Institute, 21 Union Street, 3rd Floor, Troy, New York, NY 12180, USA  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1687-8337 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:20652045; PMCID:PMC2905913 Approved no  
  Call Number IDA @ john @ Serial 291  
Permanent link to this record
 

 
Author (down) Cope, K.L.; Schook, M.W.; Benard, M.F. url  doi
openurl 
  Title Exposure to artificial light at night during the larval stage has delayed effects on juvenile corticosterone concentration in American toads, Anaxyrus americanus Type Journal Article
  Year 2020 Publication General and Comparative Endocrinology Abbreviated Journal Gen Comp Endocrinol  
  Volume in press Issue Pages 113508  
  Keywords Animals; amphibian; anthropogenic light; carry-over effects; environmental stressor; glucocorticoid; predation  
  Abstract Artificial Light At Night (ALAN) is an environmental stressor that can disrupt individual physiology and ecological interactions. Hormones such as corticosterone are often responsible for mediating an organism's response to environmental stressors. We investigated whether ALAN was associated with a corticosterone response and whether it exacerbated the effects of another common stressor, predation. We tested for consumptive, non-consumptive, and physiological effects of ALAN and predator presence (dragonfly larvae) on a widespread amphibian, the American toad (Anaxyrus americanus). We found predators had consumptive (decreased survival) and non-consumptive (decreased growth) effects on larval toads. ALAN did not affect larval toads nor did it interact with the predator treatment to increase larval toad predation. Despite the consumptive and non-consumptive effects of predators, neither predators nor ALAN affected corticosterone concentration in the larval and metamorph life-stages. In contrast to studies in other organisms, we did not find any evidence that suggested ALAN alters predator-prey interactions between dragonfly larvae and toads. However, there was an inverse relationship between corticosterone and survival that was exacerbated by exposure to ALAN when predators were absent. Additionally, larval-stage exposure to ALAN increased corticosterone concentration in juvenile toads. Our results suggest the physiological effects of ALAN may not be demonstrated until later life-stages.  
  Address Department of Biology, Case Western Reserve University, 10900 Euclid Ave., Cleveland, OH 44016, USA. Electronic address: mfb38@case.edu  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0016-6480 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:32442544 Approved no  
  Call Number GFZ @ kyba @ Serial 2931  
Permanent link to this record
 

 
Author (down) Chellappa, S.L.; Viola, A.U.; Schmidt, C.; Bachmann, V.; Gabel, V.; Maire, M.; Reichert, C.F.; Valomon, A.; Gotz, T.; Landolt, H.-P.; Cajochen, C. url  doi
openurl 
  Title Human melatonin and alerting response to blue-enriched light depend on a polymorphism in the clock gene PER3 Type Journal Article
  Year 2012 Publication The Journal of Clinical Endocrinology and Metabolism Abbreviated Journal J Clin Endocrinol Metab  
  Volume 97 Issue 3 Pages E433-7  
  Keywords Adult; Alleles; Cross-Over Studies; Female; Genotype; Homozygote; Humans; *Light; Male; Melatonin/*blood/genetics; *Minisatellite Repeats; Period Circadian Proteins/*genetics; *Polymorphism, Genetic; Questionnaires; Sleep/genetics; Wakefulness/*genetics  
  Abstract CONTEXT: Light exposure, particularly at the short-wavelength range, triggers several nonvisual responses in humans. However, the extent to which the melatonin-suppressing and alerting effect of light differs among individuals remains unknown. OBJECTIVE: Here we investigated whether blue-enriched polychromatic light impacts differentially on melatonin and subjective and objective alertness in healthy participants genotyped for the PERIOD3 (PER3) variable-number, tandem-repeat polymorphism. DESIGN, SETTING, AND PARTICIPANTS: Eighteen healthy young men homozygous for the PER3 polymorphism (PER3(5/5)and PER3(4/4)) underwent a balanced crossover design during the winter season, with light exposure to compact fluorescent lamps of 40 lux at 6500 K and at 2500 K during 2 h in the evening. RESULTS: In comparison to light at 2500 K, blue-enriched light at 6500 K induced a significant suppression of the evening rise in endogenous melatonin levels in PER3(5/5) individuals but not in PER3(4/4). Likewise, PER3(5/5) individuals exhibited a more pronounced alerting response to light at 6500 K than PER3(4/4) volunteers. Waking electroencephalographic activity in the theta range (5-7 Hz), a putative correlate of sleepiness, was drastically attenuated during light exposure at 6500 K in PER3(5/5) individuals as compared with PER3(4/4). CONCLUSIONS: We provide first evidence that humans homozygous for the PER3 5/5 allele are particularly sensitive to blue-enriched light, as indexed by the suppression of endogenous melatonin and waking theta activity. Light sensitivity in humans may be modulated by a clock gene polymorphism implicated in the sleep-wake regulation.  
  Address Centre for Chronobiology, Psychiatric Hospital of the University of Basel, Wilhelm Kleinstrasse 27, CH-4012 Basel, Switzerland  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0021-972X ISBN Medium  
  Area Expedition Conference  
  Notes PMID:22188742 Approved no  
  Call Number IDA @ john @ Serial 301  
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