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Author (down) Wyse, C.A.; Selman, C.; Page, M.M.; Coogan, A.N.; Hazlerigg, D.G.
Title Circadian desynchrony and metabolic dysfunction; did light pollution make us fat? Type Journal Article
Year 2011 Publication Medical Hypotheses Abbreviated Journal Med Hypotheses
Volume 77 Issue 6 Pages 1139-1144
Keywords Human Health; Animals; Chronobiology Disorders/*complications/etiology; History, 20th Century; History, 21st Century; Humans; Lighting/*adverse effects/history/statistics & numerical data; Metabolic Diseases/*complications/etiology; Mice; *Models, Biological; Obesity/*epidemiology/*etiology; *Photoperiod; Rats
Abstract Circadian rhythms are daily oscillations in physiology and behaviour that recur with a period of 24h, and that are entrained by the daily photoperiod. The cycle of sunrise and sunset provided a reliable time cue for many thousands of years, until the advent of artificial lighting disrupted the entrainment of human circadian rhythms to the solar photoperiod. Circadian desynchrony (CD) occurs when endogenous rhythms become misaligned with daily photoperiodic cycles, and this condition is facilitated by artificial lighting. This review examines the hypothesis that chronic CD that has accompanied the availability of electric lighting in the developed world induces a metabolic and behavioural phenotype that is predisposed to the development of obesity. The evidence to support this hypothesis is based on epidemiological data showing coincidence between the appearance of obesity and the availability of artificial light, both geographically, and historically. This association links CD to obesity in humans, and is corroborated by experimental studies that demonstrate that CD can induce obesity and metabolic dysfunction in humans and in rodents. This association between CD and obesity has far reaching implications for human health, lifestyle and work practices. Attention to the rhythmicity of daily sleep, exercise, work and feeding schedules could be beneficial in targeting or reversing the modern human predisposition to obesity.
Address Institute of Biological and Environmental Sciences, University of Aberdeen, Aberdeen AB24 3TZ, UK. c.wyse@abdn.ac.uk
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 0306-9877 ISBN Medium
Area Expedition Conference
Notes PMID:21983352 Approved no
Call Number LoNNe @ kagoburian @ Serial 837
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Author (down) Reiter, R.J.; Tan, D.-X.; Korkmaz, A.; Ma, S.
Title Obesity and metabolic syndrome: association with chronodisruption, sleep deprivation, and melatonin suppression Type Journal Article
Year 2012 Publication Annals of Medicine Abbreviated Journal Ann Med
Volume 44 Issue 6 Pages 564-577
Keywords Human Health; Adolescent; Adult; Animals; Child; Chronobiology Disorders/*epidemiology; Comorbidity; Disease Models, Animal; Humans; Light/adverse effects; Melatonin/*deficiency/physiology; Metabolic Syndrome X/*epidemiology; Mice; Obesity/*epidemiology; Rats; Sleep Deprivation/*epidemiology
Abstract Obesity has become an epidemic in industrialized and developing countries. In 30 years, unless serious changes are made, a majority of adults and many children will be classified as overweight or obese. Whereas fatness alone endangers physiological performance of even simple tasks, the associated co-morbidity of obesity including metabolic syndrome in all its manifestations is a far more critical problem. If the current trend continues as predicted, health care systems may be incapable of handling the myriad of obesity-related diseases. The financial costs, including those due to medical procedures, absenteeism from work, and reduced economic productivity, will jeopardize the financial well-being of industries. The current review summarizes the potential contributions of three processes that may be contributing to humans becoming progressively more overweight: circadian or chronodisruption, sleep deficiency, and melatonin suppression. Based on the information provided in this survey, life-style factors (independent of the availability of abundant calorie-rich foods) may aggravate weight gain. Both epidemiological and experimental data support associations between disrupted physiological rhythms, a reduction in adequate sleep, and light-at-night-induced suppression of an essential endogenously produced molecule, melatonin. The implication is that if these problems were corrected with life-style changes, body-weight could possibly be more easily controlled.
Address Department of Cellular and Structural Biology, UT Health Science Center, San Antonio, Texas, USA. reiter@uthscsa.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 0785-3890 ISBN Medium
Area Expedition Conference
Notes PMID:21668294 Approved no
Call Number LoNNe @ christopher.kyba @ Serial 523
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Author (down) Park, Y.-M.M.; White, A.J.; Jackson, C.L.; Weinberg, C.R.; Sandler, D.P.
Title Association of Exposure to Artificial Light at Night While Sleeping With Risk of Obesity in Women Type Journal Article
Year 2019 Publication JAMA Internal Medicine Abbreviated Journal JAMA Intern Med
Volume 179 Issue 8 Pages 1061-1071
Keywords Human Health; Obesity; Sleep
Abstract Importance: Short sleep has been associated with obesity, but to date the association between exposure to artificial light at night (ALAN) while sleeping and obesity is unknown. Objective: To determine whether ALAN exposure while sleeping is associated with the prevalence and risk of obesity. Design, Setting, and Participants: This baseline and prospective analysis included women aged 35 to 74 years enrolled in the Sister Study in all 50 US states and Puerto Rico from July 2003 through March 2009. Follow-up was completed on August 14, 2015. A total of 43722 women with no history of cancer or cardiovascular disease who were not shift workers, daytime sleepers, or pregnant at baseline were included in the analysis. Data were analyzed from September 1, 2017, through December 31, 2018. Exposures: Artificial light at night while sleeping reported at enrollment, categorized as no light, small nightlight in the room, light outside the room, and light or television in the room. Main Outcomes and Measures: Prevalent obesity at baseline was based on measured general obesity (body mass index [BMI] >/=30.0) and central obesity (waist circumference [WC] >/=88 cm, waist-to-hip ratio [WHR] >/=0.85, or waist-to-height ratio [WHtR]>/=0.5). To evaluate incident overweight and obesity, self-reported BMI at enrollment was compared with self-reported BMI at follow-up (mean [SD] follow-up, 5.7 [1.0] years). Generalized log-linear models with robust error variance were used to estimate multivariable-adjusted prevalence ratios (PRs) and relative risks (RRs) with 95% CIs for prevalent and incident obesity. Results: Among the population of 43 722 women (mean [SD] age, 55.4 [8.9] years), having any ALAN exposure while sleeping was positively associated with a higher prevalence of obesity at baseline, as measured using BMI (PR, 1.03; 95% CI, 1.02-1.03), WC (PR, 1.12; 95% CI, 1.09-1.16), WHR (PR, 1.04; 95% CI, 1.00-1.08), and WHtR (PR, 1.07; 95% CI, 1.04-1.09), after adjusting for confounding factors, with P < .001 for trend for each measure. Having any ALAN exposure while sleeping was also associated with incident obesity (RR, 1.19; 95% CI, 1.06-1.34). Compared with no ALAN, sleeping with a television or a light on in the room was associated with gaining 5 kg or more (RR, 1.17; 95% CI, 1.08-1.27; P < .001 for trend), a BMI increase of 10% or more (RR, 1.13; 95% CI, 1.02-1.26; P = .04 for trend), incident overweight (RR, 1.22; 95% CI,1.06-1.40; P = .03 for trend), and incident obesity (RR, 1.33; 95% CI, 1.13-1.57; P < .001 for trend). Results were supported by sensitivity analyses and additional multivariable analyses including potential mediators such as sleep duration and quality, diet, and physical activity. Conclusions and Relevance: These results suggest that exposure to ALAN while sleeping may be a risk factor for weight gain and development of overweight or obesity. Further prospective and interventional studies could help elucidate this association and clarify whether lowering exposure to ALAN while sleeping can promote obesity prevention.
Address Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina
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 2168-6106 ISBN Medium
Area Expedition Conference
Notes PMID:31180469 Approved no
Call Number GFZ @ kyba @ Serial 2525
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Author (down) Owens, B.
Title Obesity: heavy sleepers Type Journal Article
Year 2013 Publication Nature Abbreviated Journal Nature
Volume 497 Issue 7450 Pages S8-9
Keywords Human Health; Animals; Body Mass Index; CLOCK Proteins/genetics/metabolism; Circadian Rhythm/physiology; Energy Metabolism/*physiology; Ghrelin/metabolism; Humans; Insulin Resistance/physiology; Leptin/metabolism; Male; Mice; Obesity/*physiopathology; Satiety Response/physiology; Sleep/*physiology; Suprachiasmatic Nucleus/physiology; Time Factors; Weight Gain/physiology; Weight Loss/physiology
Abstract
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 0028-0836 ISBN Medium
Area Expedition Conference
Notes PMID:23698508 Approved no
Call Number LoNNe @ christopher.kyba @ Serial 503
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Author (down) Oike, H.; Sakurai, M.; Ippoushi, K.; Kobori, M.
Title Time-fixed feeding prevents obesity induced by chronic advances of light/dark cycles in mouse models of jet-lag/shift work Type Journal Article
Year 2015 Publication Biochemical and Biophysical Research Communications Abbreviated Journal Biochem Biophys Res Commun
Volume 465 Issue 3 Pages 556-561
Keywords Animals; *Circadian Clocks; *Disease Models, Animal; *Feeding Behavior; Jet Lag Syndrome/*physiopathology; Male; Mice; Mice, Inbred C57BL; Obesity/etiology/*physiopathology/*prevention & control; Photoperiod; Circadian rhythm; Clock genes; Jet lag; Metabolic disorders; Obesity; Shift work
Abstract Recent findings have uncovered intimate relationships between circadian clocks and energy metabolism. Epidemiological studies have shown that the frequency of obesity and metabolic disorders increases among shift-workers. Here we found that a chronic shift in light/dark (LD) cycles comprising an advance of six hours twice weekly, induced obesity in mice. Under such conditions that imitate jet lag/shift work, body weight and glucose intolerance increased, more fat accumulated in white adipose tissues and the expression profiles of metabolic genes changed in the liver compared with normal LD conditions. Mice fed at a fixed 12 h under the LD shift notably did not develop symptoms of obesity despite isocaloric intake. These results suggest that jet lag/shift work induces obesity as a result of fluctuating feeding times and it can be prevented by fixing meal times. This rodent model of obesity might serve as a useful tool for understanding why shift work induces metabolic disorders.
Address Food Function Division, National Food Research Institute, National Agriculture and Food Research Organization (NARO), 2-1-12 Kannondai, Tsukuba, Ibaraki 305-8642, Japan; oike(at)affrc.go.jp
Corporate Author Thesis
Publisher Elsevier Place of Publication Editor
Language English Summary Language English Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0006-291X ISBN Medium
Area Expedition Conference
Notes PMID:26297949 Approved no
Call Number IDA @ john @ Serial 1318
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