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Author (up) Figueiro, M.G.; Wood, B.; Plitnick, B.; Rea, M.S.
Title The impact of watching television on evening melatonin levels: Impact of watching television on evening melatonin Type Journal Article
Year 2013 Publication Journal of the Society for Information Display Abbreviated Journal Jnl Soc Info Display
Volume 21 Issue 10 Pages 417-421
Keywords Human Health; television; correlated color temperature; sleep; melatonin levels; blue light; circadian disruption
Abstract Self-luminous electronic devices emit optical radiation at short wavelengths, close to the peak sensitivity of melatonin suppression. The present paper investigated if light from a 178-cm (70 in.) television suppressed melatonin. Results showed that light from televisions does not impact melatonin levels in the evening.
Address
Corporate Author Thesis
Publisher Place of Publication Editor
Language Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1071-0922 ISBN Medium
Area Expedition Conference
Notes Approved no
Call Number LoNNe @ christopher.kyba @ Serial 498
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Author (up) Fonken, L.K.; Aubrecht, T.G.; Melendez-Fernandez, O.H.; Weil, Z.M.; Nelson, R.J.
Title Dim light at night disrupts molecular circadian rhythms and increases body weight Type Journal Article
Year 2013 Publication Journal of Biological Rhythms Abbreviated Journal J Biol Rhythms
Volume 28 Issue 4 Pages 262-271
Keywords Animals; Blood Glucose/metabolism; Body Weight/*physiology; CLOCK Proteins/biosynthesis/genetics; Circadian Rhythm/*physiology; Corticosterone/metabolism; Feeding Behavior/physiology; Immunohistochemistry; Light; *Lighting; Male; Mice; Motor Activity; Polymerase Chain Reaction; Suprachiasmatic Nucleus/metabolism/physiology; clock genes; feeding rhythm; light pollution; obesity
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.
Address Department of Neuroscience and Institute for Behavioral Medicine Research, Wexner Medical Center, The Ohio State University, Columbus, OH 43210, USA. 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 0748-7304 ISBN Medium
Area Expedition Conference
Notes PMID:23929553; PMCID:PMC4033305 Approved no
Call Number IDA @ john @ Serial 28
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Author (up) 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 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
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Author (up) Fonken, L.K.; Nelson, R.J.
Title Dim light at night increases depressive-like responses in male C3H/HeNHsd mice Type Journal Article
Year 2013 Publication Behavioural Brain Research Abbreviated Journal Behav Brain Res
Volume 243 Issue Pages 74-78
Keywords Affect/physiology; Anhedonia/physiology; Animals; Behavior, Animal/*physiology; Circadian Rhythm/*physiology; Depression/*etiology/physiopathology; Hippocampus/*metabolism/pathology; Light/*adverse effects; Male; Mice; Mice, Inbred C3H; Neuropsychological Tests; Photoperiod
Abstract Daily patterns of light exposure have become increasingly variable since the widespread adoption of electrical lighting during the 20th century. Seasonal fluctuations in light exposure, shift-work, and transmeridian travel are all associated with alterations in mood. These studies implicate fluctuations in environmental lighting in the development of depressive disorders. Here we argue that exposure to light at night (LAN) may be causally linked to depression. Male C3H/HeNHsd mice, which produce nocturnal melatonin, were housed in either a standard light/dark (LD) cycle or exposed to nightly dim (5 lux) LAN (dLAN). After four weeks in lighting conditions mice underwent behavioral testing and hippocampal tissue was collected at the termination of the study for qPCR. Here were report that mice exposed to dLAN increase depressive-like responses in both a sucrose anhedonia and forced swim test. In contrast to findings in diurnal grass rats, dLAN mice perform comparably to mice housed under dark nights in a hippocampus-dependent learning and memory task. TNFalpha and IL1beta gene expression do not differ between groups, demonstrating that changes in these pro-inflammatory cytokines do not mediate dLAN induced depressive-like responses in mice. BDNF expression is reduced in the hippocampus of mice exposed to dLAN. These results indicate that low levels of LAN can alter mood in mice. This study along with previous work implicates LAN as a potential factor contributing to depression. Further understanding of the mechanisms through which LAN contributes to changes in mood is important for characterizing and treating depressive disorders.
Address Department of Neuroscience, Institute for Behavioral Medicine Research, Wexner Medical Center, The Ohio State University, Columbus, OH 43210, USA. 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 0166-4328 ISBN Medium
Area Expedition Conference
Notes PMID:23291153 Approved no
Call Number IDA @ john @ Serial 95
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Author (up) Fonken, L.K.; Weil, Z.M.; Nelson, R.J.
Title Dark nights reverse metabolic disruption caused by dim light at night Type Journal Article
Year 2013 Publication Obesity (Silver Spring, Md.) Abbreviated Journal Obesity (Silver Spring)
Volume 21 Issue 6 Pages 1159-1164
Keywords Animals; Body Mass Index; Energy Intake; Gene Expression; Glucose Tolerance Test; *Light; Male; Mice; Obesity/*epidemiology/etiology; *Photoperiod; Weight Gain
Abstract OBJECTIVE: The increasing prevalence of obesity and related metabolic disorders coincides with increasing exposure to light at night. Previous studies report that mice exposed to dim light at night (dLAN) develop symptoms of metabolic syndrome. This study investigated whether mice returned to dark nights after dLAN exposure recover metabolic function. DESIGN AND METHODS: Male Swiss-Webster mice were assigned to either: standard light-dark (LD) conditions for 8 weeks (LD/LD), dLAN for 8 weeks (dLAN/dLAN), LD for 4 weeks followed by 4 weeks of dLAN (LD/dLAN), and dLAN for 4 weeks followed by 4 weeks of LD (dLAN/LD). RESULTS: After 4 weeks in their respective lighting conditions both groups initially placed in dLAN increased body mass gain compared to LD mice. Half of the dLAN mice (dLAN/LD) were then transferred to LD and vice versa (LD/dLAN). Following the transfer dLAN/dLAN and LD/dLAN mice gained more weight than LD/LD and dLAN/LD mice. At the conclusion of the study dLAN/LD mice did not differ from LD/LD mice with respect to weight gain and had lower fat pad mass compared to dLAN/dLAN mice. Compared to all other groups dLAN/dLAN mice decreased glucose tolerance as indicated by an intraperitoneal glucose tolerance test at week 7, indicating that dLAN/LD mice recovered glucose metabolism. dLAN/dLAN mice also increased MAC1 mRNA expression in peripheral fat as compared to both LD/LD and dLAN/LD mice, suggesting peripheral inflammation is induced by dLAN, but not sustained after return to LD. CONCLUSION: These results suggest that re-exposure to dark nights ameliorates metabolic disruption caused by dLAN exposure.
Address Department of Neuroscience and Institute for Behavioral Medicine Research, Wexner Medical Center, Ohio State University, Columbus, Ohio 43210, USA. 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 1930-7381 ISBN Medium
Area Expedition Conference
Notes PMID:23666854 Approved no
Call Number IDA @ john @ Serial 167
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