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Author Figueiro, M.G.; Rea, M.S.
Title The effects of red and blue lights on circadian variations in cortisol, alpha amylase, and melatonin Type Journal Article
Year 2010 Publication International Journal of Endocrinology Abbreviated Journal Int J Endocrinol
Volume (down) 2010 Issue Pages 829351
Keywords blue light; red light; circadian rhythm; cortisol; alpha amylase; melatonin; photobiology; suprachiasmatic nuclei; endocrinology
Abstract The primary purpose of the present study was to expand our understanding of the impact of light exposures on the endocrine and autonomic systems as measured by acute cortisol, alpha amylase, and melatonin responses. We utilized exposures from narrowband long-wavelength (red) and from narrow-band short-wavelength (blue) lights to more precisely understand the role of the suprachiasmatic nuclei (SCN) in these responses. In a within-subjects experimental design, twelve subjects periodically received one-hour corneal exposures of 40 lux from the blue or from the red lights while continuously awake for 27 hours. Results showed-that, as expected, only the blue light reduced nocturnal melatonin. In contrast, both blue and red lights affected cortisol levels and, although less clear, alpha amylase levels as well. The present data bring into question whether the nonvisual pathway mediating nocturnal melatonin suppression is the same as that mediating other responses to light exhibited by the endocrine and the autonomic nervous systems.
Address Lighting Research Center, Rensselaer Polytechnic Institute, 21 Union Street, 3rd Floor, Troy, New York, NY 12180, USA
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 1687-8337 ISBN Medium
Area Expedition Conference
Notes PMID:20652045; PMCID:PMC2905913 Approved no
Call Number IDA @ john @ Serial 291
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Author Arendt, J.; Middleton, B.
Title Human seasonal and circadian studies in Antarctica (Halley, 75 degrees S) Type Journal Article
Year 2018 Publication General and Comparative Endocrinology Abbreviated Journal Gen Comp Endocrinol
Volume (down) 258 Issue Pages 250-258
Keywords Human Activities; Acclimatization/*physiology; Actigraphy; Adult; Antarctic Regions; Behavior/*physiology; Circadian Rhythm/*physiology; Darkness; Female; Heart Rate/physiology; Humans; Libido; Light; Male; Melatonin/blood; Photoperiod; *Seasons; Sleep/physiology; Young Adult; *Antarctica; *Circadian; *Light; *Melatonin; *Seasonal
Abstract Living for extended periods in Antarctica exposes base personnel to extremes of daylength (photoperiod) and temperature. At the British Antarctic Survey base of Halley, 75 degrees S, the sun does not rise for 110 d in the winter and does not set for 100 d in summer. Photoperiod is the major time cue governing the timing of seasonal events such as reproduction in many species. The neuroendocrine signal providing photoperiodic information to body physiology is the duration of melatonin secretion which reflects the length of the night: longer in the short days of winter and shorter in summer. Light of sufficient intensity and spectral composition serves to suppress production of melatonin and to set the circadian timing and the duration of the rhythm. In humans early observations suggested that bright (>2000 lux) white light was needed to suppress melatonin completely. Shortly thereafter winter depression (Seasonal Affective Disorder or SAD) was described, and its successful treatment by an artificial summer photoperiod of bright white light, sufficient to shorten melatonin production. At Halley dim artificial light intensity during winter was measured, until 2003, at a maximum of approximately 500 lux in winter. Thus a strong seasonal and circadian time cue was absent. It seemed likely that winter depression would be common in the extended period of winter darkness and could be treated with an artificial summer photoperiod. These observations, and predictions, inspired a long series of studies regarding human seasonal and circadian status, and the effects of light treatment, in a small overwintering, isolated community, living in the same conditions for many months at Halley. We found little evidence of SAD, or change in duration of melatonin production with season. However the timing of the melatonin rhythm itself, and/or that of its metabolite 6-sulphatoxymelatonin (aMT6s), was used as a primary marker of seasonal, circadian and treatment changes. A substantial phase delay of melatonin in winter was advanced to summer phase by a two pulse 'skeleton' bright white light treatment. Subsequently a single morning pulse of bright white light was effective with regard to circadian phase and improved daytime performance. The circadian delay evidenced by melatonin was accompanied by delayed sleep (logs and actigraphy): poor sleep is a common complaint in Polar regions. Appropriate extra artificial light, both standard white, and blue enriched, present throughout the day, effectively countered delay in sleep timing and the aMT6s rhythm. The most important factor appeared to be the maximum light experienced. Another manifestation of the winter was a decline in self-rated libido (men only on base at this time). Women on the base showed lower aspects of physical and mental health compared to men. Free-running rhythms were seen in some subjects following night shift, but were rarely found at other times, probably because this base has strongly scheduled activity and leisure time. Complete circadian adaptation during a week of night shift, also seen in a similar situation on North Sea oil rigs, led to problems readapting back to day shift in winter, compared to summer. Here again timed light treatment was used to address the problem. Sleep, alertness and waking performance are critically dependent on optimum circadian phase. Circadian desynchrony is associated with increased risk of major disease in shift workers. These studies provide some groundwork for countering/avoiding circadian desynchrony in rather extreme conditions.
Address Biochemistry and Physiology, Faculty of Health and Medical Sciences, University of Surrey, Guildford GU2 7XH, UK. Electronic address: b.middleton@surrey.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 0016-6480 ISBN Medium
Area Expedition Conference
Notes PMID:28526480 Approved no
Call Number IDA @ john @ Serial 2248
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Author Ikeno, T.; Weil, Z.M.; Nelson, R.J.
Title Dim light at night disrupts the short-day response in Siberian hamsters Type Journal Article
Year 2014 Publication General and Comparative Endocrinology Abbreviated Journal Gen Comp Endocrinol
Volume (down) 197 Issue Pages 56-64
Keywords 2,4-dinitro-1-flourobenzene; Dnfb; Dth; Eya3; Eyes absent 3; GnIH; GnRH; Immune function; Ld; Lps; Light pollution; Pt; Pelage; Per1; Period1; Photoperiodism; Rfrp; RFamide-related peptide; Scn; Sd; Seasonality; Tsh; TSH receptor; Tshr; dLAN; delayed-type hypersensitivity; dim light at night; gonadotropin-inhibiting hormone; gonadotropin-releasing hormone; lipopolysaccharide; long days; pars tuberalis; short days; suprachiasmatic nuclei; thyroid-stimulating hormone
Abstract Photoperiodic regulation of physiology, morphology, and behavior is crucial for many animals to survive seasonally variable conditions unfavorable for reproduction and survival. The photoperiodic response in mammals is mediated by nocturnal secretion of melatonin under the control of a circadian clock. However, artificial light at night caused by recent urbanization may disrupt the circadian clock, as well as the photoperiodic response by blunting melatonin secretion. Here we examined the effect of dim light at night (dLAN) (5lux of light during the dark phase) on locomotor activity rhythms and short-day regulation of reproduction, body mass, pelage properties, and immune responses of male Siberian hamsters. Short-day animals reduced gonadal and body mass, decreased spermatid nuclei and sperm numbers, molted to a whiter pelage, and increased pelage density compared to long-day animals. However, animals that experienced short days with dLAN did not show these short-day responses. Moreover, short-day specific immune responses were altered in dLAN conditions. The nocturnal activity pattern was blunted in dLAN hamsters, consistent with the observation that dLAN changed expression of the circadian clock gene, Period1. In addition, we demonstrated that expression levels of genes implicated in the photoperiodic response, Mel-1a melatonin receptor, Eyes absent 3, thyroid stimulating hormone receptor, gonadotropin-releasing hormone, and gonadotropin-inhibitory hormone, were higher in dLAN animals than those in short-day animals. These results suggest that dLAN disturbs the circadian clock function and affects the molecular mechanisms of the photoperiodic response.
Address Department of Neuroscience, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA. Electronic address: randy.nelson@osumc.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 0016-6480 ISBN Medium
Area Expedition Conference
Notes PMID:24362257 Approved no
Call Number IDA @ john @ Serial 82
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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.
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 (down) 157 Issue 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
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:27802074 Approved no
Call Number LoNNe @ kyba @ Serial 1550
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Author Fonken, L.K.; Lieberman, R.A.; Weil, Z.M.; Nelson, R.J.
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 (down) 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