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Author Anisimov, V. N.
Title Light pollution, reproductive function and cancer risk Type Journal Article
Year 2006 Publication Neuroendocrinology Letters Abbreviated Journal
Volume 27 Issue (up) 1-2 Pages 35-52
Keywords Human Health
Abstract At present, light pollution (exposure to light-at-night) both in the form of occupational exposure during night work and as a personal choice and life style, is experienced by numerous night-active members of our society. Disruption of the circadian rhythms induced by light pollution has been associated with cancer in humans. There are epidemiological evidences of increased breast and colon cancer risk in shift workers. An inhibition of the pineal gland function with exposure to the constant light (LL) regimen promoted carcinogenesis whereas the light deprivation inhibits the carcinogenesis. Treatment with pineal indole hormone melatonin inhibits carcinogenesis in pinealectomized rats or animals kept at the standard light/dark regimen (LD) or at the LL regimen. These observations might lead to use melatonin for cancer prevention in groups of humans at risk of light pollution.
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Call Number LoNNe @ kagoburian @ Serial 703
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Author Fonken, L.K.; Lieberman, R.A.; Weil, Z.M.; Nelson, R.J.
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 (up) 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
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ISSN 0013-7227 ISBN Medium
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Notes PMID:23861373 Approved no
Call Number IDA @ john @ Serial 93
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Author Mendez, N.; Halabi, D.; Spichiger, C.; Salazar, E.R.; Vergara, K.; Alonso-Vasquez, P.; Carmona, P.; Sarmiento, J.M.; Richter, H.G.; Seron-Ferre, M.; Torres-Farfan, C.
Title Gestational Chronodisruption Impairs Circadian Physiology in Rat Male Offspring, Increasing the Risk of Chronic Disease Type Journal Article
Year 2016 Publication Endocrinology Abbreviated Journal Endocrinology
Volume 157 Issue (up) 12 Pages 4654-4668
Keywords Animals
Abstract Chronic exposure to light at night, as in shift work, alters biological clocks (chronodisruption), impacting negatively pregnancy outcome in human. Actually, the interaction of maternal and fetal circadian systems could be a key factor determining a fitting health in adult. We propose that chronic photoperiod shifts (CPS) during pregnancy, alter maternal circadian rhythms, and impair circadian physiology in the adult offspring, increasing health risks. Pregnant rats were exposed to normal photoperiod (12h-light/12h-dark) or to CSP until 85 gestation. The effects of gestational CPS were evaluated on the mother and adult offspring. In the mother we measured rhythms of heart-rate, body temperature and activity through gestation, and daily rhythms of plasma variables: melatonin, corticosterone, aldosterone and markers of renal function; at 18 days of gestation. In adult offspring, we measured rhythms of clock gene expression in the suprachiasmatic nucleus (SCN), locomotor activity, body temperature, heart rate, blood pressure, plasma variables, glucose tolerance and corticosterone response to adrenocorticotropic hormone (ACTH). CPS altered all maternal circadian rhythms; lengthened gestation and increased newborn weight. The adult CPS offspring presented normal rhythms of clock gene expression in the SCN, locomotor activity and body temperature. However, the daily rhythm of plasma melatonin was absent, and corticosterone, aldosterone, renal markers, blood pressure and heart-rate rhythms were altered. Moreover, CPS offspring presented decreased glucose tolerance and abnormal corticosterone response to ACTH. Altogether, these data shows that gestational CPS induced long-term effects on the offspring circadian system, wherein a normal SCN coexists with altered endocrine, cardiovascular and metabolic function.
Address Laboratory of Developmental Chronobiology, Institute of Anatomy, Histology and Pathology and
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ISSN 0013-7227 ISBN Medium
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Notes PMID:27802074 Approved no
Call Number LoNNe @ kyba @ Serial 1550
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Author 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.
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 (up) 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
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ISSN 0021-972X ISBN Medium
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Notes PMID:21193540; PMCID:PMC3047226 Approved no
Call Number IDA @ john @ Serial 139
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Author 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.
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 (up) 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
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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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