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Author Fonken, L.K.; Workman, J.L.; Walton, J.C.; Weil, Z.M.; Morris, J.S.; Haim, A.; Nelson, R.J. url  doi
openurl 
  Title Light at night increases body mass by shifting the time of food intake Type Journal Article
  Year (down) 2010 Publication Proceedings of the National Academy of Sciences of the United States of America Abbreviated Journal Proc Natl Acad Sci U S A  
  Volume 107 Issue 43 Pages 18664-18669  
  Keywords Animals; Body Mass Index; *Circadian Rhythm; Disease Models, Animal; Eating/*physiology/psychology/*radiation effects; Energy Intake; Feeding Behavior/physiology/psychology/radiation effects; Glucose Tolerance Test; Humans; Male; Metabolic Syndrome X/etiology; Mice; Motor Activity; Obesity/*etiology/pathology/physiopathology/psychology; *Photoperiod  
  Abstract The global increase in the prevalence of obesity and metabolic disorders coincides with the increase of exposure to light at night (LAN) and shift work. Circadian regulation of energy homeostasis is controlled by an endogenous biological clock that is synchronized by light information. To promote optimal adaptive functioning, the circadian clock prepares individuals for predictable events such as food availability and sleep, and disruption of clock function causes circadian and metabolic disturbances. To determine whether a causal relationship exists between nighttime light exposure and obesity, we examined the effects of LAN on body mass in male mice. Mice housed in either bright (LL) or dim (DM) LAN have significantly increased body mass and reduced glucose tolerance compared with mice in a standard (LD) light/dark cycle, despite equivalent levels of caloric intake and total daily activity output. Furthermore, the timing of food consumption by DM and LL mice differs from that in LD mice. Nocturnal rodents typically eat substantially more food at night; however, DM mice consume 55.5% of their food during the light phase, as compared with 36.5% in LD mice. Restricting food consumption to the active phase in DM mice prevents body mass gain. These results suggest that low levels of light at night disrupt the timing of food intake and other metabolic signals, leading to excess weight gain. These data are relevant to the coincidence between increasing use of light at night and obesity in humans.  
  Address Department of Neuroscience, 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 0027-8424 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:20937863; PMCID:PMC2972983 Approved no  
  Call Number IDA @ john @ Serial 169  
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Author Garaulet, M.; Ordovas, J.M.; Madrid, J.A. url  doi
openurl 
  Title The chronobiology, etiology and pathophysiology of obesity Type Journal Article
  Year (down) 2010 Publication International Journal of Obesity (2005) Abbreviated Journal Int J Obes (Lond)  
  Volume 34 Issue 12 Pages 1667-1683  
  Keywords Human Health; Animals; CLOCK Proteins/genetics/*physiology; Circadian Rhythm/genetics/*physiology; Energy Intake/*physiology; Feeding Behavior/physiology; Humans; Mice; Motor Activity/physiology; *Obesity/etiology/physiopathology; Sleep/physiology; Sleep Deprivation/complications/genetics/*physiopathology  
  Abstract The effect of CD on human health is an emerging issue. Many records link CD with diseases such as cancer, cardiovascular, cognitive impairment and obesity, all of them conducive to premature aging. The amount of sleep has declined by 1.5 h over the past century, accompanied by an important increase in obesity. Shift work, sleep deprivation and exposure to bright light at night increase the prevalence of adiposity. Animal models have shown that mice with Clock gene disruption are prone to developing obesity and MetS. This review summarizes the latest developments with regard to chronobiology and obesity, considering (1) how molecular clocks coordinate metabolism and the specific role of the adipocyte; (2) CD and its causes and pathological consequences; (3) the epidemiological evidence of obesity as a chronobiological illness; and (4) theories of circadian disruption and obesity. Energy intake and expenditure, relevance of sleep, fat intake from a circadian perspective and psychological and genetic aspects of obesity are examined. Finally, ideas about the use of chronobiology in the treatment of obesity are discussed. Such knowledge has the potential to become a valuable tool in the understanding of the relationship between the chronobiology, etiology and pathophysiology of obesity.  
  Address Faculty of Biology, Department of Physiology, Campus of Espinardo, University of Murcia, Murcia, Spain. garaulet@um.es  
  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 0307-0565 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:20567242 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 755  
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