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Author Cope, K.L.; Schook, M.W.; Benard, M.F.
Title Exposure to artificial light at night during the larval stage has delayed effects on juvenile corticosterone concentration in American toads, Anaxyrus americanus Type Journal Article
Year 2020 Publication General and Comparative Endocrinology Abbreviated Journal Gen Comp Endocrinol
Volume in press Issue Pages 113508
Keywords Animals; amphibian; anthropogenic light; carry-over effects; environmental stressor; glucocorticoid; predation
Abstract Artificial Light At Night (ALAN) is an environmental stressor that can disrupt individual physiology and ecological interactions. Hormones such as corticosterone are often responsible for mediating an organism's response to environmental stressors. We investigated whether ALAN was associated with a corticosterone response and whether it exacerbated the effects of another common stressor, predation. We tested for consumptive, non-consumptive, and physiological effects of ALAN and predator presence (dragonfly larvae) on a widespread amphibian, the American toad (Anaxyrus americanus). We found predators had consumptive (decreased survival) and non-consumptive (decreased growth) effects on larval toads. ALAN did not affect larval toads nor did it interact with the predator treatment to increase larval toad predation. Despite the consumptive and non-consumptive effects of predators, neither predators nor ALAN affected corticosterone concentration in the larval and metamorph life-stages. In contrast to studies in other organisms, we did not find any evidence that suggested ALAN alters predator-prey interactions between dragonfly larvae and toads. However, there was an inverse relationship between corticosterone and survival that was exacerbated by exposure to ALAN when predators were absent. Additionally, larval-stage exposure to ALAN increased corticosterone concentration in juvenile toads. Our results suggest the physiological effects of ALAN may not be demonstrated until later life-stages.
Address Department of Biology, Case Western Reserve University, 10900 Euclid Ave., Cleveland, OH 44016, USA. Electronic address: mfb38@case.edu
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 0016-6480 ISBN Medium
Area Expedition Conference
Notes PMID:32442544 Approved no
Call Number GFZ @ kyba @ Serial (down) 2931
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Author Stock, D.; Schernhammer, E.
Title Does night work affect age at which menopause occurs? Type Journal Article
Year 2019 Publication Current Opinion in Endocrinology, Diabetes, and Obesity Abbreviated Journal Curr Opin Endocrinol Diabetes Obes
Volume 26 Issue 6 Pages 306–312
Keywords Human Health; Review; shift work; Menopause; women
Abstract PURPOSE OF REVIEW: To delineate the current state of evidence on the impact of night shift work on age at natural menopause. RECENT FINDINGS: The only direct evidence is from a single observational study, which indicates that women who work night shifts are at moderately higher risk for earlier menopause and that this risk is more pronounced among younger women. Underlying biological mechanisms have yet to be sufficiently substantiated. A long-held line of inquiry, most strongly propagated by the observed link between night shift work and female breast cancer, is the 'Light at Night' hypothesis, which suggests melatonin-mediated circadian disruption as a potential regulator of reproductive signaling in women. Supporting evidence is found from observations of changes in endogenous melatonin production among night working women or in response to light exposure, and corresponding changes in endogenous ovarian hormone levels and modulated menstrual patterns, among other indications of altered central ovulation-governing processes. Susceptibility to night shift work may be modified by chronotype. SUMMARY: This review summarizes the literature related to night work and ovulatory regulation in humans, prioritizing population-based evidence to provide motivation for the study of circadian disruption and night shift work as a regulator of menopausal timing.
Address Department of Epidemiology, Center for Public Health, Medical University of Vienna, Vienna, Austria
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Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1752-296X ISBN Medium
Area Expedition Conference
Notes PMID:31644468 Approved no
Call Number GFZ @ kyba @ Serial (down) 2708
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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 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
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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 (down) 2248
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Author Jan Stenvers, D.; Scheer, F.A.J.L.; Schrauwen, P.; la Fleur, S.E.; Kalsbeek, A.
Title Circadian clocks and insulin resistance Type Journal Article
Year 2018 Publication Nature Reviews. Endocrinology Abbreviated Journal Nat Rev Endocrinol
Volume in press Issue Pages
Keywords Human Health; Review
Abstract Insulin resistance is a main determinant in the development of type 2 diabetes mellitus and a major cause of morbidity and mortality. The circadian timing system consists of a central brain clock in the hypothalamic suprachiasmatic nucleus and various peripheral tissue clocks. The circadian timing system is responsible for the coordination of many daily processes, including the daily rhythm in human glucose metabolism. The central clock regulates food intake, energy expenditure and whole-body insulin sensitivity, and these actions are further fine-tuned by local peripheral clocks. For instance, the peripheral clock in the gut regulates glucose absorption, peripheral clocks in muscle, adipose tissue and liver regulate local insulin sensitivity, and the peripheral clock in the pancreas regulates insulin secretion. Misalignment between different components of the circadian timing system and daily rhythms of sleep-wake behaviour or food intake as a result of genetic, environmental or behavioural factors might be an important contributor to the development of insulin resistance. Specifically, clock gene mutations, exposure to artificial light-dark cycles, disturbed sleep, shift work and social jet lag are factors that might contribute to circadian disruption. Here, we review the physiological links between circadian clocks, glucose metabolism and insulin sensitivity, and present current evidence for a relationship between circadian disruption and insulin resistance. We conclude by proposing several strategies that aim to use chronobiological knowledge to improve human metabolic health.
Address Netherlands Institute for Neuroscience (NIN), Royal Dutch Academy of Arts and Sciences (KNAW), Amsterdam, Netherlands. a.kalsbeek@nin.knaw.nl
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 1759-5029 ISBN Medium
Area Expedition Conference
Notes PMID:30531917 Approved no
Call Number GFZ @ kyba @ Serial (down) 2133
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Author Buonfiglio, D.; Parthimos, R.; Dantas, R.; Cerqueira Silva, R.; Gomes, G.; Andrade-Silva, J.; Ramos-Lobo, A.; Amaral, F.G.; Matos, R.; Sinesio, J.J.; Motta-Teixeira, L.C.; Donato, J.J.; Reiter, R.J.; Cipolla-Neto, J.
Title Melatonin Absence Leads to Long-Term Leptin Resistance and Overweight in Rats Type Journal Article
Year 2018 Publication Frontiers in Endocrinology Abbreviated Journal Front Endocrinol (Lausanne)
Volume 9 Issue Pages 122
Keywords Human health
Abstract Melatonin (Mel), a molecule that conveys photoperiodic information to the organisms, is also involved in the regulation of energy homeostasis. Mechanisms of action of Mel in the energy balance remain unclear; herein we investigated how Mel regulates energy intake and expenditure to promote a proper energy balance. Male Wistar rats were assigned to control, control + Mel, pinealectomized (PINX) and PINX + Mel groups. To restore a 24-h rhythm, Mel (1 mg/kg) was added to the drinking water exclusively during the dark phase for 13 weeks. After this treatment period, rats were subjected to a 24-h fasting test, an acute leptin responsiveness test and cold challenge. Mel treatment reduced food intake, body weight, and adiposity. When challenged to 24-h fasting, Mel-treated rats also showed reduced hyperphagia when the food was replaced. Remarkably, PINX rats exhibited leptin resistance; this was likely related to the capacity of leptin to affect body weight, food intake, and hypothalamic signal-transducer and activator of transcription 3 phosphorylation, all of which were reduced. Mel treatment restored leptin sensitivity in PINX rats. An increased hypothalamic expression of agouti-related peptide (Agrp), neuropeptide Y, and Orexin was observed in the PINX group while Mel treatment reduced the expression of Agrp and Orexin. In addition, PINX rats presented lower UCP1 protein levels in the brown adipose tissue and required higher tail vasoconstriction to get a proper thermogenic response to cold challenge. Our findings reveal a previously unrecognized interaction of Mel and leptin in the hypothalamus to regulate the energy balance. These findings may help to explain the high incidence of metabolic diseases in individuals exposed to light at night.
Address Department of Physiology and Biophysics, Institute of Biomedical Sciences-I, University of Sao Paulo (USP), Sao Paulo, Brazil
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 1664-2392 ISBN Medium
Area Expedition Conference
Notes PMID:29636725; PMCID:PMC5881424 Approved no
Call Number NC @ ehyde3 @ Serial (down) 2093
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