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Author 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 Evans, J.A.; Elliott, J.A.; Gorman, M.R. url  doi
openurl 
  Title Dim nighttime illumination accelerates adjustment to timezone travel in an animal model Type Journal Article
  Year 2009 Publication Current Biology : CB Abbreviated Journal Curr Biol  
  Volume 19 Issue 4 Pages R156-7  
  Keywords *Adaptation, Physiological; Animals; Behavior, Animal/physiology; Biological Clocks/*physiology; Circadian Rhythm/*physiology; Cricetinae; Humans; *Lighting; Mesocricetus; Mice; Motor Activity/physiology; Phodopus; *Photoperiod; Time Factors  
  Abstract Jetlag reflects a mismatch between local and circadian time following rapid timezone travel [1]. Appropriately timed bright light can shift human circadian rhythms but recovery is slow (e.g., 1-2 days per timezone). Most symptoms subside after resynchronization, but chronic jetlag may have enduring negative effects [2], including even accelerated mortality in mice [3]. Melatonin, prescription drugs, and/or exercise may help shift the clock but, like bright light, require complex schedules of application [1]. Thus, there is a need for more efficient and practical treatments for addressing jetlag. In contrast to bright daytime lighting, nighttime conditions have received scant attention. By incorporating more naturalistic nighttime lighting comparable in intensity to dim moonlight, we demonstrate that recovery after simulated jetlag is accelerated when nights are dimly lit rather than completely dark.  
  Address  
  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 0960-9822 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:19243688 Approved no  
  Call Number IDA @ john @ Serial 152  
Permanent link to this record
 

 
Author Froy, O.; Gotter, A.L.; Casselman, A.L.; Reppert, S.M. url  doi
openurl 
  Title Illuminating the circadian clock in monarch butterfly migration Type Journal Article
  Year 2003 Publication Science (New York, N.Y.) Abbreviated Journal Science  
  Volume 300 Issue 5623 Pages 1303-1305  
  Keywords Animals; *Animal Migration; Biological Clocks/*physiology; Butterflies/genetics/*physiology; Circadian Rhythm/*physiology; Cloning, Molecular; Darkness; Flight, Animal; Light; Nuclear Proteins/genetics/physiology; Period Circadian Proteins; Solar System; Ultraviolet Rays; butterflies; monarch  
  Abstract Migratory monarch butterflies use a time-compensated Sun compass to navigate to their overwintering grounds in Mexico. Here, we report that constant light, which disrupts circadian clock function at both the behavioral and molecular levels in monarchs, also disrupts the time-compensated component of flight navigation. We further show that ultraviolet light is important for flight navigation but is not required for photic entrainment of circadian rhythms. Tracing these distinct light-input pathways into the brain should aid our understanding of the clock-compass mechanisms necessary for successful migration.  
  Address Department of Neurobiology, University of Massachusetts Medical School, LRB-728, 364 Plantation Street, Worcester, MA 01605, 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 0036-8075 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:12764200 Approved no  
  Call Number IDA @ john @ Serial 1072  
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Author Kempinger, L.; Dittmann, R.; Rieger, D.; Helfrich-Forster, C. url  doi
openurl 
  Title The nocturnal activity of fruit flies exposed to artificial moonlight is partly caused by direct light effects on the activity level that bypass the endogenous clock Type Journal Article
  Year 2009 Publication Chronobiology International Abbreviated Journal Chronobiol Int  
  Volume 26 Issue 2 Pages 151-166  
  Keywords ARNTL Transcription Factors; Animals; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism; Behavior, Animal/physiology; Biological Clocks/*physiology; CLOCK Proteins; Circadian Rhythm/*physiology; Darkness; Drosophila Proteins/genetics/metabolism; Drosophila melanogaster/*physiology; *Light; *Moon; Motor Activity/*physiology; Nuclear Proteins/genetics/metabolism; Period Circadian Proteins; Photoperiod; Transcription Factors/genetics/metabolism  
  Abstract Artificial moonlight was recently shown to shift the endogenous clock of fruit flies and make them nocturnal. To test whether this nocturnal activity is partly due to masking effects of light, we exposed the clock-mutants per(01), tim(01), per(01);tim(01), cyc(01), and Clk(JRK) to light/dark and light/dim-light cycles and determined the activity level during the day and night. We found that under moonlit nights, all clock mutants shifted their activity significantly into the night, suggesting that this effect is independent of the clock. We also recorded the flies under continuous artificial moonlight and darkness to judge the effect of dim constant light on the activity level. All mutants, except Clk(JRK) flies, were significantly more active under artificial moonlight conditions than under complete darkness. Unexpectedly, we found residual rhythmicity of per(01) and especially tim(01) mutants under these conditions, suggesting that TIM and especially PER retained some activity in the absence of its respective partner. Nevertheless, as even the double mutants and the cyc(01) and Clk(JRK) mutants shifted their activity into the night, we conclude that dim light stimulates the activity of fruit flies in a clock-independent manner. Thus, nocturnal light has a twofold influence on flies: it shifts the circadian clock, and it increases nocturnal activity independently of the clock. The latter was also observed in some primates by others and might therefore be of a more general validity.  
  Address Institute of Zoology, University of Regensburg, Regensburg, 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 0742-0528 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:19212834 Approved no  
  Call Number IDA @ john @ Serial 113  
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Author Kovac, J.; Husse, J.; Oster, H. url  doi
openurl 
  Title A time to fast, a time to feast: the crosstalk between metabolism and the circadian clock Type Journal Article
  Year 2009 Publication Molecules and Cells Abbreviated Journal Mol Cells  
  Volume 28 Issue 2 Pages 75-80  
  Keywords Human Health; Animals; Biological Clocks/*physiology; CLOCK Proteins/genetics/metabolism; Circadian Rhythm/*physiology; Energy Metabolism/*physiology; Gene Expression Regulation; Homeostasis; Humans; Period Circadian Proteins/genetics/metabolism; Time Factors  
  Abstract The cyclic environmental conditions brought about by the 24 h rotation of the earth have allowed the evolution of endogenous circadian clocks that control the temporal alignment of behaviour and physiology, including the uptake and processing of nutrients. Both metabolic and circadian regulatory systems are built upon a complex feedback network connecting centres of the central nervous system and different peripheral tissues. Emerging evidence suggests that circadian clock function is closely linked to metabolic homeostasis and that rhythm disruption can contribute to the development of metabolic disease. At the same time, metabolic processes feed back into the circadian clock, affecting clock gene expression and timing of behaviour. In this review, we summarize the experimental evidence for this bimodal interaction, with a focus on the molecular mechanisms mediating this exchange, and outline the implications for clock-based and metabolic diseases.  
  Address Circadian Rhythms Group, Max Planck Institute of Biophysical Chemistry, 37077, 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 1016-8478 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:19714310 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 772  
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