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Author Zhang, L.; Zhang, Z.; Wang, F.; Tian, X.; Ji, P.; Liu, G. url  doi
openurl 
  Title Effects of melatonin administration on embryo implantation and offspring growth in mice under different schedules of photoperiodic exposure Type Journal Article
  Year 2017 Publication Reproductive Biology and Endocrinology : RB&E Abbreviated Journal Reprod Biol Endocrinol  
  Volume 15 Issue (up) 1 Pages 78  
  Keywords Animals  
  Abstract BACKGROUND: Embryo implantation is crucial for animal reproduction. Unsuccessful embryo implantation leads to pregnancy failure, especially in human-assisted conception. Environmental factors have a profound impact on embryo implantation. Because people are being exposed to more light at night, the influence of long-term light exposure on embryo implantation should be explored. METHODS: The effects of long photoperiodic exposure and melatonin on embryo implantation and offspring growth were examined. Long photoperiodic exposure (18:6 h light:dark) was selected to resemble light pollution. Melatonin (10-2, 10-3, 10-4, 10-5 M) was added to the drinking water of mice starting at Day 1 (vaginal plugs) until delivery. RESULTS: Melatonin treatment (10-4,10-5 M) significantly increased litter sizes compared to untreated controls (12.9 +/- 0.40 and 12.2 +/- 1.01 vs. 11.5 +/- 0.43; P < 0.05). The most effective concentration of melatonin (10-4 M) was selected for further investigation. No remarkable differences were found between melatonin-treated mice and controls in terms of the pups' birth weights, weaning survival rates, and weaning weights. Long photoperiodic exposure significantly reduced the number of implantation sites in treated mice compared to controls (light/dark, 12/12 h), and melatonin rescued this negative effect. Mechanistic studies revealed that melatonin enhanced the serum 17beta-estradiol (E2) levels in the pregnant mice and upregulated the expression of the receptors MT1 and MT2 and p53 in uterine tissue. All of these factors may contribute to the beneficial effects of melatonin on embryo implantation in mice. CONCLUSION: Melatonin treatment was associated with beneficial effects in pregnant mice, especially those subjected to long photoperiodic exposure. This was achieved by enhanced embryo implantation. At the molecular level, melatonin administration probably increases the E2 level during pregnancy and upregulates p53 expression by activating MT1/2 in the uterus. All of the changes may improve the microenvironment of the uterus and, thus, the outcomes of pregnancy.  
  Address State Key Laboratory of Animal Nutrition, Key Laboratory of Animal Genetics and Breeding of the Ministry of Agriculture, National Engineering Laboratory for Animal Breeding, College of Animal Science and Technology, China Agricultural University, Beijing, 100193, China. gshliu@cau.edu.cn  
  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 1477-7827 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28969693 Approved no  
  Call Number LoNNe @ kyba @ Serial 1751  
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Author Anisimov, V. N. url  openurl
  Title Light pollution, reproductive function and cancer risk Type Journal Article
  Year 2006 Publication Neuroendocrinology Letters Abbreviated Journal  
  Volume 27 Issue (up) 1-2 Pages 35-52  
  Keywords Human Health  
  Abstract At present, light pollution (exposure to light-at-night) both in the form of occupational exposure during night work and as a personal choice and life style, is experienced by numerous night-active members of our society. Disruption of the circadian rhythms induced by light pollution has been associated with cancer in humans. There are epidemiological evidences of increased breast and colon cancer risk in shift workers. An inhibition of the pineal gland function with exposure to the constant light (LL) regimen promoted carcinogenesis whereas the light deprivation inhibits the carcinogenesis. Treatment with pineal indole hormone melatonin inhibits carcinogenesis in pinealectomized rats or animals kept at the standard light/dark regimen (LD) or at the LL regimen. These observations might lead to use melatonin for cancer prevention in groups of humans at risk of light pollution.  
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  Notes Approved no  
  Call Number LoNNe @ kagoburian @ Serial 703  
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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 (up) 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  
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  Language English Summary Language Original Title  
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  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 Mendez, N.; Halabi, D.; Spichiger, C.; Salazar, E.R.; Vergara, K.; Alonso-Vasquez, P.; Carmona, P.; Sarmiento, J.M.; Richter, H.G.; Seron-Ferre, M.; Torres-Farfan, C. url  doi
openurl 
  Title Gestational Chronodisruption Impairs Circadian Physiology in Rat Male Offspring, Increasing the Risk of Chronic Disease Type Journal Article
  Year 2016 Publication Endocrinology Abbreviated Journal Endocrinology  
  Volume 157 Issue (up) 12 Pages 4654-4668  
  Keywords Animals  
  Abstract Chronic exposure to light at night, as in shift work, alters biological clocks (chronodisruption), impacting negatively pregnancy outcome in human. Actually, the interaction of maternal and fetal circadian systems could be a key factor determining a fitting health in adult. We propose that chronic photoperiod shifts (CPS) during pregnancy, alter maternal circadian rhythms, and impair circadian physiology in the adult offspring, increasing health risks. Pregnant rats were exposed to normal photoperiod (12h-light/12h-dark) or to CSP until 85 gestation. The effects of gestational CPS were evaluated on the mother and adult offspring. In the mother we measured rhythms of heart-rate, body temperature and activity through gestation, and daily rhythms of plasma variables: melatonin, corticosterone, aldosterone and markers of renal function; at 18 days of gestation. In adult offspring, we measured rhythms of clock gene expression in the suprachiasmatic nucleus (SCN), locomotor activity, body temperature, heart rate, blood pressure, plasma variables, glucose tolerance and corticosterone response to adrenocorticotropic hormone (ACTH). CPS altered all maternal circadian rhythms; lengthened gestation and increased newborn weight. The adult CPS offspring presented normal rhythms of clock gene expression in the SCN, locomotor activity and body temperature. However, the daily rhythm of plasma melatonin was absent, and corticosterone, aldosterone, renal markers, blood pressure and heart-rate rhythms were altered. Moreover, CPS offspring presented decreased glucose tolerance and abnormal corticosterone response to ACTH. Altogether, these data shows that gestational CPS induced long-term effects on the offspring circadian system, wherein a normal SCN coexists with altered endocrine, cardiovascular and metabolic function.  
  Address Laboratory of Developmental Chronobiology, Institute of Anatomy, Histology and Pathology and  
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  Series Volume Series Issue Edition  
  ISSN 0013-7227 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:27802074 Approved no  
  Call Number LoNNe @ kyba @ Serial 1550  
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Author Gooley, J.J.; Chamberlain, K.; Smith, K.A.; Khalsa, S.B.S.; Rajaratnam, S.M.W.; Van Reen, E.; Zeitzer, J.M.; Czeisler, C.A.; Lockley, S.W. url  doi
openurl 
  Title Exposure to room light before bedtime suppresses melatonin onset and shortens melatonin duration in humans Type Journal Article
  Year 2011 Publication The Journal of Clinical Endocrinology and Metabolism Abbreviated Journal J Clin Endocrinol Metab  
  Volume 96 Issue (up) 3 Pages E463-72  
  Keywords Adolescent; Adult; Female; Humans; *Light; *Lighting; Male; Melatonin/*blood; Sleep/physiology; Time Factors; Young Adult  
  Abstract CONTEXT: Millions of individuals habitually expose themselves to room light in the hours before bedtime, yet the effects of this behavior on melatonin signaling are not well recognized. OBJECTIVE: We tested the hypothesis that exposure to room light in the late evening suppresses the onset of melatonin synthesis and shortens the duration of melatonin production. DESIGN: In a retrospective analysis, we compared daily melatonin profiles in individuals living in room light (<200 lux) vs. dim light (<3 lux). PATIENTS: Healthy volunteers (n = 116, 18-30 yr) were recruited from the general population to participate in one of two studies. SETTING: Participants lived in a General Clinical Research Center for at least five consecutive days. INTERVENTION: Individuals were exposed to room light or dim light in the 8 h preceding bedtime. OUTCOME MEASURES: Melatonin duration, onset and offset, suppression, and phase angle of entrainment were determined. RESULTS: Compared with dim light, exposure to room light before bedtime suppressed melatonin, resulting in a later melatonin onset in 99.0% of individuals and shortening melatonin duration by about 90 min. Also, exposure to room light during the usual hours of sleep suppressed melatonin by greater than 50% in most (85%) trials. CONCLUSIONS: These findings indicate that room light exerts a profound suppressive effect on melatonin levels and shortens the body's internal representation of night duration. Hence, chronically exposing oneself to electrical lighting in the late evening disrupts melatonin signaling and could therefore potentially impact sleep, thermoregulation, blood pressure, and glucose homeostasis.  
  Address Division of Sleep Medicine, Brigham and Women's Hospital and Harvard Medical School, 221 Longwood Avenue, Boston, Massachusetts 02115, USA. gmsjjg@nus.edu  
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  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0021-972X ISBN Medium  
  Area Expedition Conference  
  Notes PMID:21193540; PMCID:PMC3047226 Approved no  
  Call Number IDA @ john @ Serial 139  
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