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Author (up) Barclay, J.L.; Husse, J.; Bode, B.; Naujokat, N.; Meyer-Kovac, J.; Schmid, S.M.; Lehnert, H.; Oster, H. url  doi
openurl 
  Title Circadian desynchrony promotes metabolic disruption in a mouse model of shiftwork Type Journal Article
  Year 2012 Publication PloS one Abbreviated Journal PLoS One  
  Volume 7 Issue 5 Pages e37150  
  Keywords Animals; Biological Clocks/*physiology; Circadian Rhythm/*physiology; Disease Models, Animal; Eating/genetics; Gene Expression Regulation; Liver/metabolism; Male; Mice; Sleep Disorders, Circadian Rhythm/*metabolism/physiopathology; Suprachiasmatic Nucleus/*metabolism; Transcriptome  
  Abstract Shiftwork is associated with adverse metabolic pathophysiology, and the rising incidence of shiftwork in modern societies is thought to contribute to the worldwide increase in obesity and metabolic syndrome. The underlying mechanisms are largely unknown, but may involve direct physiological effects of nocturnal light exposure, or indirect consequences of perturbed endogenous circadian clocks. This study employs a two-week paradigm in mice to model the early molecular and physiological effects of shiftwork. Two weeks of timed sleep restriction has moderate effects on diurnal activity patterns, feeding behavior, and clock gene regulation in the circadian pacemaker of the suprachiasmatic nucleus. In contrast, microarray analyses reveal global disruption of diurnal liver transcriptome rhythms, enriched for pathways involved in glucose and lipid metabolism and correlating with first indications of altered metabolism. Although altered food timing itself is not sufficient to provoke these effects, stabilizing peripheral clocks by timed food access can restore molecular rhythms and metabolic function under sleep restriction conditions. This study suggests that peripheral circadian desynchrony marks an early event in the metabolic disruption associated with chronic shiftwork. Thus, strengthening the peripheral circadian system by minimizing food intake during night shifts may counteract the adverse physiological consequences frequently observed in human shift workers.  
  Address Max Planck Institute of Biophysical Chemistry, Gottingen, Germany  
  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 1932-6203 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:22629359; PMCID:PMC3357388 Approved no  
  Call Number IDA @ john @ Serial 94  
Permanent link to this record
 

 
Author (up) Bedrosian, T.A.; Vaughn, C.A.; Galan, A.; Daye, G.; Weil, Z.M.; Nelson, R.J. url  doi
openurl 
  Title Nocturnal light exposure impairs affective responses in a wavelength-dependent manner Type Journal Article
  Year 2013 Publication The Journal of Neuroscience : the Official Journal of the Society for Neuroscience Abbreviated Journal J Neurosci  
  Volume 33 Issue 32 Pages 13081-13087  
  Keywords Analysis of Variance; Animals; Circadian Rhythm/*physiology; Cricetinae; Dose-Response Relationship, Radiation; Female; Food Deprivation/physiology; Food Preferences/physiology/radiation effects; Fourier Analysis; Gene Expression Regulation/radiation effects; Hippocampus/pathology/radiation effects; Immobility Response, Tonic/radiation effects; Light/*adverse effects; Mood Disorders/*etiology/pathology; Motor Activity/physiology/radiation effects; Phodopus; Proto-Oncogene Proteins c-fos/metabolism; Social Behavior; Suprachiasmatic Nucleus/metabolism; Time Factors  
  Abstract Life on earth is entrained to a 24 h solar cycle that synchronizes circadian rhythms in physiology and behavior; light is the most potent entraining cue. In mammals, light is detected by (1) rods and cones, which mediate visual function, and (2) intrinsically photosensitive retinal ganglion cells (ipRGCs), which primarily project to the suprachiasmatic nucleus (SCN) in the hypothalamus to regulate circadian rhythms. Recent evidence, however, demonstrates that ipRGCs also project to limbic brain regions, suggesting that, through this pathway, light may have a role in cognition and mood. Therefore, it follows that unnatural exposure to light may have negative consequences for mood or behavior. Modern environmental lighting conditions have led to excessive exposure to light at night (LAN), and particularly to blue wavelength lights. We hypothesized that nocturnal light exposure (i.e., dim LAN) would induce depressive responses and alter neuronal structure in hamsters (Phodopus sungorus). If this effect is mediated by ipRGCs, which have reduced sensitivity to red wavelength light, then we predicted that red LAN would have limited effects on brain and behavior compared with shorter wavelengths. Additionally, red LAN would not induce c-Fos activation in the SCN. Our results demonstrate that exposure to LAN influences behavior and neuronal plasticity and that this effect is likely mediated by ipRGCs. Modern sources of LAN that contain blue wavelengths may be particularly disruptive to the circadian system, potentially contributing to altered mood regulation.  
  Address Department of Neuroscience, Ohio State University Wexner Medical Center, Columbus, Ohio 43210, USA. Bedrosian.2@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 0270-6474 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23926261 Approved no  
  Call Number IDA @ john @ Serial 27  
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Author (up) Brady, A.; Willis, B.; Harder, L.; Vizel, P. url  doi
openurl 
  Title Lunar Phase Modulates Circadian Gene Expression Cycles in the Broadcast Spawning Coral Acropora millepora Type Journal Article
  Year 2016 Publication Biological Bulletin Abbreviated Journal Biol Bullet  
  Volume 230 Issue 2 Pages 130-142  
  Keywords Animals; corals; Acropora millepora; lunar cycle; Circadian Rhythm; gene expression; moon  
  Abstract Many broadcast spawning corals in multiple reef regions release their gametes with incredible temporal precision just once per year, using the lunar cycle to set the night of spawning. Moonlight, rather than tides or other lunar-regulated processes, is thought to be the proximate factor responsible for linking the night of spawning to the phase of the Moon. We compared patterns of gene expression among colonies of the broadcast spawning coral Acropora millepora at different phases of the lunar cycle, and when they were maintained under one of three experimentally simulated lunar lighting treatments: i) lunar lighting conditions matching those on the reef, or lunar patterns mimicking either ii) constant full Moon conditions, or iii) constant new Moon conditions. Normal lunar illumination was found to shift both the level and timing of clock gene transcription cycles between new and full moons, with the peak hour of expression for a number of genes occurring earlier in the evening under a new Moon when compared to a full Moon. When the normal lunar cycle is replaced with nighttime patterns equivalent to either a full Moon or a new Moon every evening, the normal monthlong changes in the level of expression are destroyed for most genes. In combination, these results indicate that daily changes in moonlight that occur over the lunar cycle are essential for maintaining normal lunar periodicity of clock gene transcription, and this may play a role in regulating spawn timing. These data also show that low levels of light pollution may have an impact on coral biological clocks.  
  Address Department of Biological Science, University of Calgary, 2500 University Drive NW, Calgary, Alberta T2N 1N4, Canada; pvize(at)ucalgary.ca  
  Corporate Author Thesis  
  Publisher Marine Biological Laboratory Place of Publication Editor  
  Language English Summary Language English Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number IDA @ john @ Serial 1476  
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Author (up) Cajochen, C.; Jud, C.; Munch, M.; Kobialka, S.; Wirz-Justice, A.; Albrecht, U. url  doi
openurl 
  Title Evening exposure to blue light stimulates the expression of the clock gene PER2 in humans Type Journal Article
  Year 2006 Publication The European Journal of Neuroscience Abbreviated Journal Eur J Neurosci  
  Volume 23 Issue 4 Pages 1082-1086  
  Keywords Human Health; Adult; Color; Darkness; Dose-Response Relationship, Radiation; Female; Gene Expression/*radiation effects; Humans; *Light; Male; Melatonin/metabolism; Mucous Membrane/metabolism/radiation effects; Nuclear Proteins/genetics/*metabolism; Period Circadian Proteins; Transcription Factors/genetics/*metabolism  
  Abstract We developed a non-invasive method to measure and quantify human circadian PER2 gene expression in oral mucosa samples and show that this gene oscillates in a circadian (= about a day) fashion. We also have the first evidence that induction of human PER2 expression is stimulated by exposing subjects to 2 h of light in the evening. This increase in PER2 expression was statistically significant in comparison to a non-light control condition only after light at 460 nm (blue) but not after light exposure at 550 nm (green). Our results indicate that the non-image-forming visual system is involved in human circadian gene expression. The demonstration of a functional circadian machinery in human buccal samples and its response to light opens the door for investigation of human circadian rhythms at the gene level and their associated disorders.  
  Address Centre for Chronobiology, Psychiatric University Clinics, University of Basel, CH-4025 Basel, Switzerland. christian.cajochen@unibas.ch  
  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 0953-816X ISBN Medium  
  Area Expedition Conference  
  Notes PMID:16519674 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 727  
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Author (up) 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  
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