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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 Review; Human Health
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 (down) Netherlands Institute for Neuroscience (NIN), Royal Dutch Academy of Arts and Sciences (KNAW), Amsterdam, Netherlands. a.kalsbeek@nin.knaw.nl
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 1759-5029 ISBN Medium
Area Expedition Conference
Notes PMID:30531917 Approved no
Call Number GFZ @ kyba @ Serial 2133
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Author Ma, Q.; Tan, Y.; Chen, X.; Chen, S.; Sun, Y.; Zhou, B.
Title Regulation of the MAPK signaling pathway by miR-421-5p in rats under light pollution Type Journal Article
Year 2018 Publication International Journal of Molecular Medicine Abbreviated Journal Int J Mol Med
Volume in press Issue Pages in press
Keywords Animals
Abstract The present study aimed to explore the difference in the expression profiles of ovarian microRNA sequences in rats in a light pollution environment and rats in a normal light environment. Rats in the control group were exposed to 12h light/dark cycles, while rats in the model group were continuously exposed to 24h light. The ovaries were extracted from the two groups of rats, and Illumina HiSeq 2500 highthroughput sequencing technology was used to detect the differences in microRNA (miRNA) expression among the two groups. Fluorescence quantitative reverse transcriptionpolymerase chain reaction was used to verify the differential expression of miRNA. The present study was designed to experimentally validate the interaction between miR4215p and mitogenactivated protein kinase (MAPK) 7 by using the dualluciferase reporter system, and to explore the expression of proteins in the MAPK signaling pathway with a lentiviral vectormediated small hairpin RNA interference against microRNA4215p. The expression of 45 miRNAs was significantly different. In total, 13 miRNAs were upregulated, of which 5 miRNA sequences were known and 8 were predicted. Furthermore, 32 miRNAs were downregulated, of which 11 miRNA sequences were known and 21 were predicted. The results of the luciferase reporter assay confirmed the targeting association between miR4215p and MAPK7. The expression levels of MAPK and genes in its downstream signaling pathways, including cFos, CREB and cMyc, were downregulated when miR4215p was overexpressed and upregulated when miR4215p was silenced. The differential expression of miRNAs may serve an important role in the development of the ovary in a light pollution environment. miR4215p may regulate ovarian growth and development by targeting the MAPK signaling pathway in light polluted rat ovaries.
Address (down) Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, P.R. China
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 1107-3756 ISBN Medium
Area Expedition Conference
Notes PMID:30221682 Approved no
Call Number GFZ @ kyba @ Serial 2005
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Author Watson, L.A.; Phillips, A.J.K.; Hosken, I.T.; McGlashan, E.M.; Anderson, C.; Lack, L.C.; Lockley, S.W.; Rajaratnam, S.M.W.; Cain, S.W.
Title Increased sensitivity of the circadian system to light in delayed sleep-wake phase disorder Type Journal Article
Year 2018 Publication The Journal of Physiology Abbreviated Journal J Physiol
Volume in press Issue Pages
Keywords Human Health
Abstract KEY POINTS: This is the first study to demonstrate an altered circadian phase shifting response in a circadian rhythm sleep disorder. Patients with Delayed Sleep-Wake Phase Disorder (DSWPD) demonstrate greater sensitivity of the circadian system to the phase delaying effects of light. Increased circadian sensitivity to light is associated with later circadian timing within both control and DSWPD groups. DSWPD patients had a greater sustained pupil response after light exposure. Treatments for DSWPD should consider sensitivity of the circadian system to light as a potential underlying vulnerability, making patients susceptible to relapse. ABSTRACT: Patients with Delayed Sleep-Wake Phase Disorder (DSWPD) exhibit delayed sleep-wake behavior relative to desired bedtime, often leading to chronic sleep restriction and daytime dysfunction. The majority of DSWPD patients also display delayed circadian timing in the melatonin rhythm. Hypersensitivity of the circadian system to phase delaying light is a plausible physiological basis for DSWPD vulnerability. We compared the phase shifting response to a 6.5-h light exposure ( approximately 150 lux) between male patients with diagnosed DSWPD (n = 10; aged 22.4 +/- 3.3 years) and male healthy controls (n = 11; aged 22.4 +/- 2.4 years). Salivary dim light melatonin onset (DLMO) was measured under controlled conditions in dim light (<3 lux) before and after light exposure. Correcting for the circadian time of the light exposure, DSWPD patients exhibited 31.5% greater phase delay shifts than healthy controls. In both groups, a later initial phase of the melatonin rhythm was associated with greater magnitude of phase shifts, indicating that increased circadian sensitivity to light may be a factor that contributes to delayed phase, even in non-clinical groups. DSWPD patients also had reduced pupil size following the light exposure, and showed a trend towards increased melatonin suppression during light exposure. These findings indicate that, for patients with DSWPD, assessment of light sensitivity may be an important factor that can inform behavioral therapy, including minimization of exposure to phase-delaying night-time light. This article is protected by copyright. All rights reserved.
Address (down) Monash Institute of Cognitive and Clinical Neurosciences, School of Psychological Sciences, Monash University, Melbourne, Victoria, Australia
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 0022-3751 ISBN Medium
Area Expedition Conference
Notes PMID:30281150 Approved no
Call Number GFZ @ kyba @ Serial 2026
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Author McGlashan, E.M.; Nandam, L.S.; Vidafar, P.; Mansfield, D.R.; Rajaratnam, S.M.W.; Cain, S.W.
Title The SSRI citalopram increases the sensitivity of the human circadian system to light in an acute dose Type Journal Article
Year 2018 Publication Psychopharmacology Abbreviated Journal Psychopharmacology (Berl)
Volume in press Issue Pages in press
Keywords Human Health
Abstract RATIONALE: Disturbances of the circadian system are common in depression. Though they typically subside when depression is treated with antidepressants, the mechanism by which this occurs is unknown. Despite being the most commonly prescribed class of antidepressants, the effect of selective serotonin reuptake inhibitors (SSRIs) on the human circadian clock is not well understood. OBJECTIVE: To examine the effect of the SSRI citalopram (30 mg) on the sensitivity of the human circadian system to light. METHODS: This study used a double-blind, placebo-controlled, within-subjects, crossover design. Participants completed two melatonin suppression assessments in room level light (~ 100 lx), taking either a single dose of citalopram 30 mg or a placebo at the beginning of each light exposure. Melatonin suppression was calculated by comparing placebo and citalopram light exposure conditions to a dim light baseline. RESULTS: A 47% increase in melatonin suppression was observed after administration of an acute dose of citalopram, with all participants showing more suppression after citalopram administration (large effect, d = 1.54). Further, melatonin onset occurred later under normal room light with citalopram compared to placebo. CONCLUSIONS: Increased sensitivity of the circadian system to light could assist in explaining some of the inter-individual variability in antidepressant treatment responses, as it is likely to assist in recovery in some patients, while causing further disruption for others.
Address (down) Monash Institute of Cognitive and Clinical Neurosciences, School of Psychological Sciences, Monash University, 18 Innovation Walk, Clayton, VIC, 3800, Australia. sean.cain@monash.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 0033-3158 ISBN Medium
Area Expedition Conference
Notes PMID:30219986 Approved no
Call Number GFZ @ kyba @ Serial 2012
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Author Giraudeau, M.; Sepp, T.; Ujvari, B.; Ewald, P.W.; Thomas, F.
Title Human activities might influence oncogenic processes in wild animal populations Type Journal Article
Year 2018 Publication Nature Ecology & Evolution Abbreviated Journal Nat Ecol Evol
Volume 2 Issue Pages 1065-1070
Keywords Commentary; Animals
Abstract Based on the abundant studies available on humans showing clear associations between rapid environmental changes and the rate of neoplasia, we propose that human activities might increase cancer rate in wild populations through numerous processes. Most of the research on this topic has concentrated on wildlife cancer prevalence in environments that are heavily contaminated with anthropogenic chemicals. Here, we propose that human activities might also increase cancer rate in wild populations through additional processes including light pollution, accidental (for example, human waste) or intentional (for example, bird feeders) wildlife feeding (and the associated change of diet), or reduction of genetic diversity in human-impacted habitats. The human species can thus be defined as an oncogenic species, moderating the environment in the way that it causes cancer in other wild populations. As human impacts on wildlife are predicted to increase rather than decrease (for example, in the context of urbanization), acknowledging the possible links between human activity and cancer in wild populations is crucial.
Address (down) MIVEGEC, Montpellier, France. frederic.thomas2@ird.fr
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 2397-334X ISBN Medium
Area Expedition Conference
Notes PMID:29784981 Approved no
Call Number GFZ @ kyba @ Serial 1921
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