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Author Anisimov, V.N.; Vinogradova, I.A.; Panchenko, A.V.; Popovich, I.G.; Zabezhinskii, M.A. url  openurl
  Title Light-at-Night-Induced Circadian Disruption, Cancer and Aging Type Journal Article
  Year 2012 Publication Current Aging Science Abbreviated Journal  
  Volume 5 Issue 3 Pages 170-177  
  Keywords Animals; Light-at-night; aging; cancer; cardiovascular diseases; circadian; circadian rhythm; diabetes; disruption; melatonin; shift-work  
  Abstract Light-at-night has become an increasing and essential part of the modern lifestyle and leads to a number of health problems, including excessive body mass index, cardiovascular diseases, diabetes, and cancer. The International Agency for Research on Cancer (IARC) Working Group concluded that “shift-work that involves circadian disruption is probably carcinogenic to humans” (Group 2A) [1]. According to the circadian disruption hypothesis, light-at-night might disrupt the endogenous circadian rhythm and specifically suppress nocturnal production of the pineal hormone melatonin and its secretion into the blood. We evaluated the effect of various light/dark regimens on the survival, life span, and spontaneous and chemical carcinogenesis in rodents. Exposure to constant illumination was followed by accelerated aging and enhanced spontaneous tumorigenesis in female CBA and transgenic HER-2/neu mice. In male and female rats maintained at various light/dark regimens (standard 12:12 light/dark [LD], the natural light [NL] of northwestern Russia, constant light [LL], and constant darkness [DD]) from the age of 25 days until natural death, it was found that exposure to NL and LL regimens accelerated age-related switch-off of the estrous function (in females), induced development of metabolic syndrome and spontaneous tumorigenesis, and shortened life span both in male and females rats compared to the standard LD regimen. Melatonin given in nocturnal drinking water prevented the adverse effect of the constant illumination (LL) and natural light (NL) regimens on the homeostasis, life span, and tumor development both in mice and rats. The exposure to the LL regimen accelerated colon carcinogenesis induced by 1,2-dimethylhydrazine (DMH) in rats, whereas the treatment with melatonin alleviated the effects of LL. The maintenance of rats at the DD regimen inhibited DMH-induced carcinogenesis. The LL regimen accelerated, whereas the DD regimen inhibited both mammary carcinogenesis induced by N-nitrosomethylurea and transplacental carcinogenesis induced by N-nitrosoethylurea in rats. Treatment with melatonin prevented premature aging and tumorigenesis in rodents. The data found in the literature and our observations suggest that the use of melatonin would be effective for cancer prevention in humans at risk as a result of light pollution.  
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  Notes Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 377  
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Author Obayashi, K.; Yamagami, Y.; Kurumatani, N.; Saeki, K. url  doi
openurl 
  Title Bedroom lighting environment and incident diabetes mellitus: a longitudinal study of the HEIJO-KYO cohort Type Journal Article
  Year 2019 Publication Sleep Medicine Abbreviated Journal Sleep Medicine  
  Volume 65 Issue Pages 1-3  
  Keywords Human Health; Metabolic disorders; diabetes; geriatrics  
  Abstract Objectives

Light information received by the brain influences human circadian timing and metabolism; low-level light at night (LAN) significantly increased body mass and led to prediabetes in mice. We hypothesized that LAN exposure increases the diabetes risk in humans. The aim of the present study was to evaluate a longitudinal association between LAN exposure and the incidence of diabetes in a general population.

Methods

In our prospective cohort study, bedroom light intensity was measured at 1-min intervals in 678 elderly participants without diabetes at baseline. The average light intensity recorded between bedtimes and rise times over two consecutive nights was used in the analysis.

Results

During follow-up (median, 42 months), 19 of the 678 participants (mean age, 70.6 years) developed diabetes. Poisson regression models revealed that the incidence rate for diabetes was significantly higher in the LAN group (average ≥5 lux, N = 128) than the dark group (average <5 lux, N = 550) (incidence rate ratio, 3.74; 95% confidence interval (CI), 1.55–9.05; p=0.003). Further propensity score adjustments in relation to LAN produced consistent results (incidence rate ratio, 3.19; 95% CI, 1.38–7.35; p=0.007). When the cut-off value of LAN was decreased to 3 lux, the relationship remained significant (incidence rate ratio 2.74; 95% CI, 1.19–6.33; p=0.018).

Conclusions

Our findings suggest that LAN exposure increases the incidence of diabetes in a general elderly population. Further research involving a large cohort with new-onset diabetes is warranted to elucidate these findings.
 
  Address Department of Epidemiology, Nara Medical University School of Medicine, 840 Shijocho, Kashiharashi, Nara, 634-8521, Japan; obayashi(at)naramed-u.ac.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 1389-9457 ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number GFZ @ kyba @ Serial 2605  
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Author Qian, J.; Scheer, F.A.J.L. url  doi
openurl 
  Title Circadian System and Glucose Metabolism: Implications for Physiology and Disease Type Journal Article
  Year 2016 Publication Trends in Endocrinology and Metabolism: TEM Abbreviated Journal Trends Endocrinol Metab  
  Volume 27 Issue 5 Pages 282-293  
  Keywords Human Health; circadian rhythms; food timing; glucose metabolism; melatonin; sleep; type 2 diabetes  
  Abstract The circadian system serves one of the most fundamental properties present in nearly all organisms: it generates 24-h rhythms in behavioral and physiological processes and enables anticipating and adapting to daily environmental changes. Recent studies indicate that the circadian system is important in regulating the daily rhythm in glucose metabolism. Disturbance of this circadian control or of its coordination relative to the environmental/behavioral cycle, such as in shift work, eating late, or due to genetic changes, results in disturbed glucose control and increased type 2 diabetes risk. Therefore, an in-depth understanding of the mechanisms underlying glucose regulation by the circadian system and its disturbance may help in the development of therapeutic interventions against the deleterious health consequences of circadian disruption.  
  Address Medical Chronobiology Program, Division of Sleep and Circadian Disorders, Brigham and Women's Hospital, Boston, MA 02115, USA; Division of Sleep Medicine, Harvard Medical School, Boston, MA 02115, USA; fscheer(at)bwh.harvard.edu  
  Corporate Author Thesis  
  Publisher Cell Place of Publication Editor  
  Language English Summary Language English Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1043-2760 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:27079518; PMCID:PMC4842150 Approved no  
  Call Number IDA @ john @ Serial 1446  
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Author Rakshit, K.; Thomas, A.P.; Matveyenko, A.V. url  doi
openurl 
  Title Does disruption of circadian rhythms contribute to beta-cell failure in type 2 diabetes? Type Journal Article
  Year 2014 Publication Current Diabetes Reports Abbreviated Journal Curr Diab Rep  
  Volume 14 Issue 4 Pages 474  
  Keywords *epidemiology; diabetes; Type 2 diabetes; beta cell; T2DM; artificial light; light exposure; circadian disruption  
  Abstract Type 2 diabetes mellitus (T2DM) is a complex metabolic disease characterized by the loss of beta-cell secretory function and mass. The pathophysiology of beta-cell failure in T2DM involves a complex interaction between genetic susceptibilities and environmental risk factors. One environmental condition that is gaining greater appreciation as a risk factor for T2DM is the disruption of circadian rhythms (eg, shift-work and sleep loss). In recent years, circadian disruption has become increasingly prevalent in modern societies and consistently shown to augment T2DM susceptibility (partly mediated through its effects on pancreatic beta-cells). Since beta-cell failure is essential for development of T2DM, we will review current work from epidemiologic, clinical, and animal studies designed to gain insights into the molecular and physiological mechanisms underlying the predisposition to beta-cell failure associated with circadian disruption. Elucidating the role of circadian clocks in regulating beta-cell health will add to our understanding of T2DM pathophysiology and may contribute to the development of novel therapeutic and preventative approaches.  
  Address Larry L. Hillblom Islet Research Center, Department of Medicine, Division of Endocrinology, University of California Los Angeles, David Geffen School of Medicine, Los Angeles, California, 900A Weyburn Place, Los Angeles, CA, 90095, USA  
  Corporate Author Thesis  
  Publisher Springer Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1534-4827 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:24532160; PMCID:PMC3988110 Approved no  
  Call Number IDA @ john @ Serial 320  
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Author Russart, K.L.G.; Chbeir, S.A.; Nelson, R.J.; Magalang, U.J. url  doi
openurl 
  Title Light at night exacerbates metabolic dysfunction in a polygenic mouse model of type 2 diabetes mellitus Type Journal Article
  Year 2019 Publication Life Sciences Abbreviated Journal Life Sci  
  Volume 231 Issue Pages 116574  
  Keywords Animals; diabetes; human health; mouse models; Type 2 diabetes; Insulin Resistance  
  Abstract AIMS: Electric lighting is beneficial to modern society; however, it is becoming apparent that light at night (LAN) is not without biological consequences. Several studies have reported negative effects of LAN on health and behavior in humans and nonhuman animals. Exposure of non-diabetic mice to dim LAN impairs glucose tolerance, whereas a return to dark nights (LD) reverses this impairment. We predicted that exposure to LAN would exacerbate the metabolic abnormalities in TALLYHO/JngJ (TH) mice, a polygenic model of type 2 diabetes mellitus (T2DM). MATERIALS AND METHODS: We exposed 7-week old male TH mice to either LD or LAN for 8-10weeks in two separate experiments. After 8weeks of light treatment, we conducted intraperitoneal glucose tolerance testing (ipGTT) followed by intraperitoneal insulin tolerance testing (ipITT). In Experiment 1, all mice were returned to LD for 4weeks, and ipITT was repeated. KEY FINDINGS: The major results of this study are i) LAN exposure for 8weeks exacerbates glucose intolerance and insulin resistance ii) the effects of LAN on insulin resistance are reversed upon return to LD, iii) LAN exposure results in a greater increase in body weight compared to LD exposure, iv) LAN increases the incidence of mice developing overt T2DM, and v) LAN exposure decreases survival of mice with T2DM. SIGNIFICANCE: In conclusion, LAN exacerbated metabolic abnormalities in a polygenic mouse model of T2DM, and these effects were reversed upon return to dark nights. The applicability of these findings to humans with T2DM needs to be determined.  
  Address Department of Neuroscience, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA; Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0024-3205 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:31207311 Approved no  
  Call Number GFZ @ kyba @ Serial 2549  
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