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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
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 (up) GFZ @ kyba @ Serial 2133
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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
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 1752-296X ISBN Medium
Area Expedition Conference
Notes PMID:31644468 Approved no
Call Number (up) GFZ @ kyba @ Serial 2708
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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
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:32442544 Approved no
Call Number (up) GFZ @ kyba @ Serial 2931
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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 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 (up) IDA @ john @ Serial 82
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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 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 (up) IDA @ john @ Serial 93
Permanent link to this record