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Author (up) Abay, K.A.; Amare, M. url  doi
openurl 
  Title Night light intensity and women's body weight: Evidence from Nigeria Type Journal Article
  Year 2018 Publication Economics and Human Biology Abbreviated Journal Econ Hum Biol  
  Volume 31 Issue Pages 238-248  
  Keywords Remote Sensing; Human Health; Adolescent; Adult; Body Mass Index; *Body Weight; Cross-Sectional Studies; Female; Health Surveys; Humans; Lighting/*statistics & numerical data; Middle Aged; Nigeria/epidemiology; Obesity/epidemiology; Overweight/*epidemiology; Prevalence; *Urbanization; Young Adult; *Bmi; *Nigeria; *Night light; *Obesity; *Overweight; *Urbanization  
  Abstract The prevalence of overweight and obesity are increasing in many African countries and hence becoming regional public health challenges. We employ satellite-based night light intensity data as a proxy for urbanization to investigate the relationship between urbanization and women's body weight. We use two rounds of the Demographic and Health Survey data from Nigeria. We employ both nonparametric and parametric estimation approaches that exploit both the cross-sectional and longitudinal variations in night light intensities. Our empirical analysis reveals nonlinear relationships between night light intensity and women's body weight measures. Doubling the sample's average level of night light intensity is associated with up to a ten percentage point increase in the probability of overweight. However, despite the generally positive relationship between night light intensity and women's body weight, the strength of the relationship varies across the assorted stages of night light intensity. Early stages of night light intensity are not significantly associated with women's body weight, while higher stages of nightlight intensities are associated with higher rates of overweight and obesity. Given that night lights are strong predictors of urbanization and related economic activities, our results hint at nonlinear relationships between various stages of urbanization and women's body weight.  
  Address International Food Policy Research Institute (IFPRI), USA. Electronic address: M.Amare@cgiar.org  
  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 1570-677X ISBN Medium  
  Area Expedition Conference  
  Notes PMID:30312904 Approved no  
  Call Number GFZ @ kyba @ Serial 2714  
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Author (up) Bray, M.S.; Young, M.E. url  doi
openurl 
  Title Chronobiological Effects on Obesity Type Journal Article
  Year 2012 Publication Current Obesity Reports Abbreviated Journal Curr Obes Rep  
  Volume 1 Issue 1 Pages 9-15  
  Keywords Human Health; Chronobiological effects; Circadian; Gene; Molecular clock; Obesity; Rhythm; Shift work; Sleep; Transcription  
  Abstract The development of obesity is the consequence of a multitude of complex interactions between both genetic and environmental factors. It has been suggested that the dramatic increase in the prevalence of obesity over the past 30 years has been the result of environmental changes that have enabled the full realization of genetic susceptibility present in the population. Among the many environmental alterations that have occurred in our recent history is the ever-increasing dyssynchrony between natural cycles of light/dark and altered patterns of sleep/wake and eating behavior associated with our “24-hour” lifestyle. An extensive research literature has established clear links between increased risk for obesity and both sleep deprivation and shift work, and our understanding of the consequences of such dyssynchrony at the molecular level is beginning to emerge. Studies linking alterations in cellular circadian clocks to metabolic dysfunction point to the increasing importance of chronobiology in obesity etiology.  
  Address Departments of Epidemiology and Genetics, University of Alabama at Birmingham, Birmingham, AL  
  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 2162-4968 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23682347; PMCID:PMC3653336 Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 510  
Permanent link to this record
 

 
Author (up) Bray, M.S.; Young, M.E. url  doi
openurl 
  Title Chronobiological Effects on Obesity Type Journal Article
  Year 2012 Publication Current Obesity Reports Abbreviated Journal Curr Obes Rep  
  Volume 1 Issue 1 Pages 9-15  
  Keywords Human Health; Chronobiological effects; Circadian; Gene; Molecular clock; Obesity; Rhythm; Shift work; Sleep; Transcription  
  Abstract The development of obesity is the consequence of a multitude of complex interactions between both genetic and environmental factors. It has been suggested that the dramatic increase in the prevalence of obesity over the past 30 years has been the result of environmental changes that have enabled the full realization of genetic susceptibility present in the population. Among the many environmental alterations that have occurred in our recent history is the ever-increasing dyssynchrony between natural cycles of light/dark and altered patterns of sleep/wake and eating behavior associated with our “24-hour” lifestyle. An extensive research literature has established clear links between increased risk for obesity and both sleep deprivation and shift work, and our understanding of the consequences of such dyssynchrony at the molecular level is beginning to emerge. Studies linking alterations in cellular circadian clocks to metabolic dysfunction point to the increasing importance of chronobiology in obesity etiology.  
  Address Departments of Epidemiology and Genetics, University of Alabama at Birmingham, Birmingham, AL  
  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 2162-4968 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23682347; PMCID:PMC3653336 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 725  
Permanent link to this record
 

 
Author (up) Cornean, R.E.; Margescu, M.; Simionescu, B. url  openurl
  Title Disruption of the Cyrcadian System and Obesity Type Journal Article
  Year 2015 Publication Jurnalul Pediatrului Abbreviated Journal Jurnalul Pediatrului  
  Volume XVIII Issue Supplement 3 Pages 38-42  
  Keywords Human Health; sleep deprivation; circadian rhythms; *Chronobiology Disorders; chronodisruption; obesity  
  Abstract Disruption of the cyrcadian system is a relatively new concept incriminated as being responsible for obesity, cardiovascular involvement, cognitive impairment, premature aging and last but not least, cancer. Because obesity is undoubtedly assimilated today to the medical conditions related to the disruption of the normal chronobiology, this paper presents the pivotal role of chronodisruption in the neuroendocrine control of appetite among these patients.  
  Address University of Medicine and Pharmacy "Iuliu Hatieganu” Cluj – Napoca, Romania; recornean(as)yahoo.com  
  Corporate Author Thesis  
  Publisher Romanian Society of Pediatric Surgery Place of Publication Editor  
  Language English Summary Language English Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 2065-4855 ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number IDA @ john @ Serial 1349  
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Author (up) Eisenstein, M. url  doi
openurl 
  Title Chronobiology: stepping out of time Type Journal Article
  Year 2013 Publication Nature Abbreviated Journal Nature  
  Volume 497 Issue 7450 Pages S10-2  
  Keywords Human Health; Animals; Benzofurans/therapeutic use; CLOCK Proteins/genetics/metabolism; Circadian Rhythm/genetics/*physiology; Cyclopropanes/therapeutic use; Efficiency/physiology; Humans; Melatonin/agonists/metabolism; Obesity/metabolism; Sleep/genetics/*physiology; Suprachiasmatic Nucleus/metabolism  
  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:23698500 Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 500  
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Author (up) Fonken, L.K.; Aubrecht, T.G.; Melendez-Fernandez, O.H.; Weil, Z.M.; Nelson, R.J. url  doi
openurl 
  Title Dim light at night disrupts molecular circadian rhythms and increases body weight Type Journal Article
  Year 2013 Publication Journal of Biological Rhythms Abbreviated Journal J Biol Rhythms  
  Volume 28 Issue 4 Pages 262-271  
  Keywords Animals; Blood Glucose/metabolism; Body Weight/*physiology; CLOCK Proteins/biosynthesis/genetics; Circadian Rhythm/*physiology; Corticosterone/metabolism; Feeding Behavior/physiology; Immunohistochemistry; Light; *Lighting; Male; Mice; Motor Activity; Polymerase Chain Reaction; Suprachiasmatic Nucleus/metabolism/physiology; clock genes; feeding rhythm; light pollution; obesity  
  Abstract With the exception of high latitudes, life has evolved under bright days and dark nights. Most organisms have developed endogenously driven circadian rhythms that are synchronized to this daily light/dark cycle. In recent years, humans have shifted away from the naturally occurring solar light cycle in favor of artificial and sometimes irregular light schedules produced by electric lighting. Exposure to unnatural light cycles is increasingly associated with obesity and metabolic syndrome; however, the means by which environmental lighting alters metabolism are poorly understood. Thus, we exposed mice to dim light at night and investigated changes in the circadian system and metabolism. Here we report that exposure to ecologically relevant levels of dim (5 lux) light at night altered core circadian clock rhythms in the hypothalamus at both the gene and protein level. Circadian rhythms in clock expression persisted during light at night; however, the amplitude of Per1 and Per2 rhythms was attenuated in the hypothalamus. Circadian oscillations were also altered in peripheral tissues critical for metabolic regulation. Exposure to dimly illuminated, as compared to dark, nights decreased the rhythmic expression in all but one of the core circadian clock genes assessed in the liver. Additionally, mice exposed to dim light at night attenuated Rev-Erb expression in the liver and adipose tissue. Changes in the circadian clock were associated with temporal alterations in feeding behavior and increased weight gain. These results are significant because they provide evidence that mild changes in environmental lighting can alter circadian and metabolic function. Detailed analysis of temporal changes induced by nighttime light exposure may provide insight into the onset and progression of obesity and metabolic syndrome, as well as other disorders involving sleep and circadian rhythm disruption.  
  Address Department of Neuroscience and Institute for Behavioral Medicine Research, Wexner Medical Center, The 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 0748-7304 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23929553; PMCID:PMC4033305 Approved no  
  Call Number IDA @ john @ Serial 28  
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Author (up) 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 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  
Permanent link to this record
 

 
Author (up) Fonken, L.K.; Weil, Z.M.; Nelson, R.J. url  doi
openurl 
  Title Dark nights reverse metabolic disruption caused by dim light at night Type Journal Article
  Year 2013 Publication Obesity (Silver Spring, Md.) Abbreviated Journal Obesity (Silver Spring)  
  Volume 21 Issue 6 Pages 1159-1164  
  Keywords Animals; Body Mass Index; Energy Intake; Gene Expression; Glucose Tolerance Test; *Light; Male; Mice; Obesity/*epidemiology/etiology; *Photoperiod; Weight Gain  
  Abstract OBJECTIVE: The increasing prevalence of obesity and related metabolic disorders coincides with increasing exposure to light at night. Previous studies report that mice exposed to dim light at night (dLAN) develop symptoms of metabolic syndrome. This study investigated whether mice returned to dark nights after dLAN exposure recover metabolic function. DESIGN AND METHODS: Male Swiss-Webster mice were assigned to either: standard light-dark (LD) conditions for 8 weeks (LD/LD), dLAN for 8 weeks (dLAN/dLAN), LD for 4 weeks followed by 4 weeks of dLAN (LD/dLAN), and dLAN for 4 weeks followed by 4 weeks of LD (dLAN/LD). RESULTS: After 4 weeks in their respective lighting conditions both groups initially placed in dLAN increased body mass gain compared to LD mice. Half of the dLAN mice (dLAN/LD) were then transferred to LD and vice versa (LD/dLAN). Following the transfer dLAN/dLAN and LD/dLAN mice gained more weight than LD/LD and dLAN/LD mice. At the conclusion of the study dLAN/LD mice did not differ from LD/LD mice with respect to weight gain and had lower fat pad mass compared to dLAN/dLAN mice. Compared to all other groups dLAN/dLAN mice decreased glucose tolerance as indicated by an intraperitoneal glucose tolerance test at week 7, indicating that dLAN/LD mice recovered glucose metabolism. dLAN/dLAN mice also increased MAC1 mRNA expression in peripheral fat as compared to both LD/LD and dLAN/LD mice, suggesting peripheral inflammation is induced by dLAN, but not sustained after return to LD. CONCLUSION: These results suggest that re-exposure to dark nights ameliorates metabolic disruption caused by dLAN exposure.  
  Address Department of Neuroscience and Institute for Behavioral Medicine Research, Wexner Medical Center, Ohio State University, Columbus, Ohio 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 1930-7381 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23666854 Approved no  
  Call Number IDA @ john @ Serial 167  
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Author (up) 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 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 (up) Garaulet, M.; Ordovas, J.M.; Madrid, J.A. url  doi
openurl 
  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 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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