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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.
Title Light at night increases body mass by shifting the time of food intake Type Journal Article
Year 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 (down) 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 Bedrosian, T.A.; Vaughn, C.A.; Galan, A.; Daye, G.; Weil, Z.M.; Nelson, R.J.
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 (down) 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 Garaulet, M.; Ordovas, J.M.; Madrid, J.A.
Title The chronobiology, etiology and pathophysiology of obesity Type Journal Article
Year 2010 Publication International Journal of Obesity (2005) Abbreviated Journal Int J Obes (Lond)
Volume 34 Issue 12 Pages (down) 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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Author Raiewski, E.E.; Elliott, J.A.; Evans, J.A.; Glickman, G.L.; Gorman, M.R.
Title Twice daily melatonin peaks in Siberian but not Syrian hamsters under 24 h light:dark:light:dark cycles Type Journal Article
Year 2012 Publication Chronobiology International Abbreviated Journal Chronobiol Int
Volume 29 Issue 9 Pages (down) 1206-1215
Keywords Animals; Circadian Rhythm/*physiology; Cricetinae; Male; Melatonin/blood/*secretion; Mesocricetus/blood/*physiology; Motor Activity/physiology; Phodopus/blood/*physiology; Photoperiod; Species Specificity
Abstract The daily pattern of blood-borne melatonin varies seasonally under the control of a multi-oscillator circadian pacemaker. Here we examine patterns of melatonin secretion and locomotor activity in Siberian and Syrian hamsters entrained to bimodal LDLD8:4:8:4 and LD20:4 lighting schedules that facilitate novel temporal arrangements of component circadian oscillators. Under LDLD, both species robustly bifurcated wheel-running activity in distinct day scotophase (DS) and night scotophase (NS) bouts. Siberian hamsters displayed significant melatonin increases during each scotophase in LDLD, and in the single daily scotophase of LD20:4. The bimodal melatonin secretion pattern persisted in acutely extended 16 h scotophases. Syrian hamsters, in contrast, showed no significant increases in plasma melatonin during either scotophase of LDLD8:4:8:4 or in LD20:4. In this species, detectable levels were observed only when the DS of LDLD was acutely extended to yield 16 h of darkness. Established species differences in the phase lag of nocturnal melatonin secretion relative to activity onset may underlie the above contrast: In non-bifurcated entrainment to 24 h LD cycles, Siberian hamsters show increased melatonin secretion within approximately 2 h after activity onset, whereas in Syrian hamsters, detectable melatonin secretion phase lags activity onset and the L/D transition by at least 4 h. The present results provide new evidence indicating multi-oscillator regulation of the waveform of melatonin secretion, specifically, the circadian control of the onset, offset and duration of nocturnal secretion.
Address Department of Psychology, and Center for Chronobiology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0109, USA. eraiewski@ucsd.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 0742-0528 ISBN Medium
Area Expedition Conference
Notes PMID:23003567 Approved no
Call Number IDA @ john @ Serial 85
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Author Sherman, H.; Gutman, R.; Chapnik, N.; Meylan, J.; le Coutre, J.; Froy, O.
Title Caffeine alters circadian rhythms and expression of disease and metabolic markers Type Journal Article
Year 2011 Publication The International Journal of Biochemistry & Cell Biology Abbreviated Journal Int J Biochem Cell Biol
Volume 43 Issue 5 Pages (down) 829-838
Keywords Human Health; Animals; Biological Markers/blood/metabolism; Body Weight/drug effects/physiology; Caffeine/*pharmacology; Caloric Restriction; Circadian Rhythm/*drug effects/genetics/physiology; *Disease/genetics; Eating/drug effects/physiology; Gene Expression Regulation/*drug effects/genetics; HEK293 Cells; Humans; Inflammation/metabolism; Male; Mice; Mice, Inbred C57BL; Motor Activity/drug effects/physiology
Abstract The circadian clock regulates many aspects of physiology, energy metabolism, and sleep. Restricted feeding (RF), a regimen that restricts the duration of food availability entrains the circadian clock. Caffeine has been shown to affect both metabolism and sleep. However, its effect on clock gene and clock-controlled gene expression has not been studied. Here, we tested the effect of caffeine on circadian rhythms and the expression of disease and metabolic markers in the serum, liver, and jejunum of mice supplemented with caffeine under ad libitum (AL) feeding or RF for 16 weeks. Caffeine significantly affected circadian oscillation and the daily levels of disease and metabolic markers. Under AL, caffeine reduced the average daily mRNA levels of certain disease and inflammatory markers, such as liver alpha fetoprotein (Afp), C-reactive protein (Crp), jejunum alanine aminotransferase (Alt), growth arrest and DNA damage 45beta (Gadd45beta), Interleukin 1alpha (Il-1alpha), Il-1beta mRNA and serum plasminogen activator inhibitor 1 (PAI-1). Under RF, caffeine reduced the average daily levels of Alt, Gadd45beta, Il-1alpha and Il-1beta mRNA in the jejunum, but not in the liver. In addition, caffeine supplementation led to decreased expression of catabolic factors under RF. In conclusion, caffeine affects circadian gene expression and metabolism possibly leading to beneficial effects mainly under AL feeding.
Address Institute of Biochemistry, Food Science and Nutrition, Robert H. Smith Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, Rehovot 76100, Israel
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 1357-2725 ISBN Medium
Area Expedition Conference
Notes PMID:21352949 Approved no
Call Number LoNNe @ kagoburian @ Serial 810
Permanent link to this record