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Author Obayashi, K.; Saeki, K.; Kurumatani, N. url  doi
openurl 
  Title Ambient Light Exposure and Changes in Obesity Parameters: A Longitudinal Study of the HEIJO-KYO Cohort Type Journal Article
  Year 2016 Publication The Journal of Clinical Endocrinology and Metabolism Abbreviated Journal J Clin Endocrinol Metab  
  Volume Issue Pages jc20154123  
  Keywords Human Health  
  Abstract (up) CONTEXT: Previous epidemiological studies have suggested an association between nighttime light levels and the prevalence of obesity, although evidence is limited to cross-sectional studies. OBJECTIVE: To evaluate the longitudinal association between ambient light exposure and the subsequent changes in obesity parameters. DESIGN AND PARTCIPANTS: Data from 1,110 elderly participants at baseline (mean age, 71.9 years) and data from 766 at follow-up (median, 21 months) were included in this prospective population-based study. MEASURES: Time-dependent ambient light exposure based on objective measurements and changes in the waist-to-height ratio (WHtR) and body mass index (BMI) were measured. RESULTS: Multivariable mixed-effect linear regression models showed a significant association between light exposure and the %WHtR gain; this was independent of potential confounders (e.g., caloric intake, physical activity, and sleep/wake parameters). Nighttime or evening exposure to higher light intensity was significantly associated with subsequent %WHtR gain. Morning exposure to a longer time >/=500 lux or nighttime exposure to a longer time <3 lux was significantly associated with subsequent %WHtR loss. These association trends were nearly consistent when the BMI was used as an obesity parameter. Increased nighttime light exposure (mean >/=3 vs. <3 lux) was estimated to correspond to a 10.2% WHtR gain and 10.0% increase in BMI over 10 years. CONCLUSIONS: Ambient light exposure, such as increased nighttime or evening light exposure and decreased morning light exposure, was independently associated with subsequent increases in obesity parameters. Further interventional studies are warranted to establish an optimal controlled lighting environment as a preventive option against obesity.  
  Address Department of Community Health and Epidemiology, Nara Medical University School of Medicine, Nara, Japan  
  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 0021-972X ISBN Medium  
  Area Expedition Conference  
  Notes PMID:27383113 Approved no  
  Call Number LoNNe @ kyba @ Serial 1483  
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Author Higuchi, S.; Nagafuchi, Y.; Lee, S.-I.; Harada, T. url  doi
openurl 
  Title Influence of Light at Night on Melatonin Suppression in Children Type Journal Article
  Year 2014 Publication The Journal of Clinical Endocrinology and Metabolism Abbreviated Journal J Clin Endocrinol Metab  
  Volume 99 Issue 9 Pages 3298-3303  
  Keywords melatonin; light at night; photobiology; children  
  Abstract (up) Context: The sensitivity of melatonin to light suppression is expected to be higher in children since children have large pupils and pure crystal lenses. However, melatonin suppression by light in children remains unclear. Objective: We investigated whether light-induced melatonin suppression in children is larger than that in adults. Methods: Thirty-three healthy primary school children (mean age: 7.4 +/- 1.8 yr) and 29 healthy adults (mean age: 41.2 +/- 4.8 yr) participated in two experiments. In the first experiment, salivary melatonin concentrations in 13 children and 13 adults were measured at night under a dim light (< 30 lx) and moderately bright light (580 lx) in an experimental facility. Pupil diameters were also measured under dim light and bright light. In the second experiment, melatonin concentrations in 20 children and 16 adults were measured under dim light in the experimental facility and under room light at home (illuminance 140.0 +/- 82.7 lx). Results: In the experiment 1, the melatonin concentration was significantly decreased by exposure to moderately bright light in both adults and children. Melatonin suppression was significantly larger in children (88.2%, n=5) than in adults (46.3%, n=6) (p<0.01), although the data for some participants were excluded because melatonin concentrations had not yet risen. In the experiment 2, melatonin secretion was significantly suppressed by room light at home in children (n=15) (p<0.05) but not in adults (n=11). Conclusion: We found that the percentage of melatonin suppression by light in children was almost twice that in adults, suggesting that melatonin in children is more sensitive than that in adults to light at night.  
  Address Department of Human Science, Faculty of Design, Kyushu University, Fukuoka, Japan  
  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 0021-972X ISBN Medium  
  Area Expedition Conference  
  Notes PMID:24840814 Approved no  
  Call Number IDA @ john @ Serial 300  
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Author Kayumov, L.; Casper, R.F.; Hawa, R.J.; Perelman, B.; Chung, S.A.; Sokalsky, S.; Shapiro, C.M. url  doi
openurl 
  Title Blocking low-wavelength light prevents nocturnal melatonin suppression with no adverse effect on performance during simulated shift work Type Journal Article
  Year 2005 Publication The Journal of Clinical Endocrinology and Metabolism Abbreviated Journal J Clin Endocrinol Metab  
  Volume 90 Issue 5 Pages 2755-2761  
  Keywords Lighting; Adult; *Circadian Rhythm; Female; Humans; *Light; Male; Melatonin/*secretion; *Work Schedule Tolerance  
  Abstract (up) Decreases in melatonin production in human and animals are known to be caused by environmental lighting, especially short-wavelength lighting (between 470 and 525 nm). We investigated the novel hypothesis that the use of goggles with selective exclusion of all wavelengths less than 530 nm could prevent the suppression of melatonin in bright-light conditions during a simulated shift-work experiment. Salivary melatonin levels were measured under dim (<5 lux), bright (800 lux), and filtered (800 lux) light at hourly intervals between 2000 and 0800 h in 11 healthy young males and eight females (mean age, 24.7 +/- 4.6 yr). The measurements were performed during three nonconsecutive nights over a 2-wk period. Subjective sleepiness was measured by self-report scales, whereas objective performance was assessed with the Continuous Performance Test. All subjects demonstrated preserved melatonin levels in filtered light similar to their dim-light secretion profile. Unfiltered bright light drastically suppressed melatonin production. Normalization of endogenous melatonin production while wearing goggles did not impair measures of performance, subjective sleepiness, or alertness.  
  Address Sleep Research Laboratory, Department of Psychiatry, University Health Network, ECW 3D-035, 399 Bathurst Street, Toronto, Ontario, Canada M5T 2S8. lkayumov@uhnres.utoronto.ca  
  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 0021-972X ISBN Medium  
  Area Expedition Conference  
  Notes PMID:15713707 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 640  
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Author 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 (up) 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 Jan Stenvers, D.; Scheer, F.A.J.L.; Schrauwen, P.; la Fleur, S.E.; Kalsbeek, A. url  doi
openurl 
  Title Circadian clocks and insulin resistance Type Journal Article
  Year 2018 Publication Nature Reviews. Endocrinology Abbreviated Journal Nat Rev Endocrinol  
  Volume in press Issue Pages  
  Keywords Human Health; Review  
  Abstract (up) Insulin resistance is a main determinant in the development of type 2 diabetes mellitus and a major cause of morbidity and mortality. The circadian timing system consists of a central brain clock in the hypothalamic suprachiasmatic nucleus and various peripheral tissue clocks. The circadian timing system is responsible for the coordination of many daily processes, including the daily rhythm in human glucose metabolism. The central clock regulates food intake, energy expenditure and whole-body insulin sensitivity, and these actions are further fine-tuned by local peripheral clocks. For instance, the peripheral clock in the gut regulates glucose absorption, peripheral clocks in muscle, adipose tissue and liver regulate local insulin sensitivity, and the peripheral clock in the pancreas regulates insulin secretion. Misalignment between different components of the circadian timing system and daily rhythms of sleep-wake behaviour or food intake as a result of genetic, environmental or behavioural factors might be an important contributor to the development of insulin resistance. Specifically, clock gene mutations, exposure to artificial light-dark cycles, disturbed sleep, shift work and social jet lag are factors that might contribute to circadian disruption. Here, we review the physiological links between circadian clocks, glucose metabolism and insulin sensitivity, and present current evidence for a relationship between circadian disruption and insulin resistance. We conclude by proposing several strategies that aim to use chronobiological knowledge to improve human metabolic health.  
  Address Netherlands Institute for Neuroscience (NIN), Royal Dutch Academy of Arts and Sciences (KNAW), Amsterdam, Netherlands. a.kalsbeek@nin.knaw.nl  
  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 1759-5029 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:30531917 Approved no  
  Call Number GFZ @ kyba @ Serial 2133  
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