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Molcan, L.; Sutovska, H.; Okuliarova, M.; Senko, T.; Krskova, L.; Zeman, M. |
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Title |
Dim light at night attenuates circadian rhythms in the cardiovascular system and suppresses melatonin in rats |
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Journal Article |
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Year |
2019 |
Publication |
Life Sciences |
Abbreviated Journal |
Life Sci |
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231 |
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116568 |
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Animals |
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Abstract |
AIMS: Cardiovascular parameters exhibit significant 24-h variability, which is coordinated by the suprachiasmatic nucleus (SCN), and light/dark cycles control SCN activity. We aimed to study the effects of light at night (ALAN; 1-2lx) on cardiovascular system control in normotensive rats. MAIN METHODS: Heart rate (HR) and blood pressure (BP) were measured by telemetry during five weeks of ALAN exposure. From beat-to-beat telemetry data, we evaluated spontaneous baroreflex sensitivity (sBRS). After 2 (A2) and 5 (A5) weeks of ALAN, plasma melatonin concentrations and the response of BP and HR to norepinephrine administration were measured. The expression of endothelial nitric oxide synthase (eNOS) and endothelin-1 was determined in the aorta. Spontaneous exploratory behaviour was evaluated in an open-field test. KEY FINDINGS: ALAN significantly suppressed the 24-h variability in the HR, BP, and sBRS after A2, although the parameters were partially restored after A5. The daily variability in the BP response to norepinephrine was reduced after A2 and restored after A5. ALAN increased the BP response to norepinephrine compared to the control after A5. Increased eNOS expression was found in arteries after A2 but not A5. Endothelin-1 expression was not affected by ALAN. Plasma melatonin levels were suppressed after A2 and A5. Spontaneous exploratory behaviour was reduced. SIGNIFICANCE: ALAN decreased plasma melatonin and the 24-h variability in the haemodynamic parameters and increased the BP response to norepinephrine. A low intensity ALAN can suppress circadian control of the cardiovascular system with negative consequences on the anticipation of a load. |
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Department of Animal Physiology and Ethology, Faculty of Natural Sciences, Comenius University, Bratislava, Slovakia |
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0024-3205 |
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PMID:31202842 |
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GFZ @ kyba @ |
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2548 |
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Russart, K.L.G.; Chbeir, S.A.; Nelson, R.J.; Magalang, U.J. |
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Title |
Light at night exacerbates metabolic dysfunction in a polygenic mouse model of type 2 diabetes mellitus |
Type |
Journal Article |
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Year |
2019 |
Publication |
Life Sciences |
Abbreviated Journal |
Life Sci |
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Volume |
231 |
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116574 |
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Keywords |
Animals; diabetes; human health; mouse models; Type 2 diabetes; Insulin Resistance |
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AIMS: Electric lighting is beneficial to modern society; however, it is becoming apparent that light at night (LAN) is not without biological consequences. Several studies have reported negative effects of LAN on health and behavior in humans and nonhuman animals. Exposure of non-diabetic mice to dim LAN impairs glucose tolerance, whereas a return to dark nights (LD) reverses this impairment. We predicted that exposure to LAN would exacerbate the metabolic abnormalities in TALLYHO/JngJ (TH) mice, a polygenic model of type 2 diabetes mellitus (T2DM). MATERIALS AND METHODS: We exposed 7-week old male TH mice to either LD or LAN for 8-10weeks in two separate experiments. After 8weeks of light treatment, we conducted intraperitoneal glucose tolerance testing (ipGTT) followed by intraperitoneal insulin tolerance testing (ipITT). In Experiment 1, all mice were returned to LD for 4weeks, and ipITT was repeated. KEY FINDINGS: The major results of this study are i) LAN exposure for 8weeks exacerbates glucose intolerance and insulin resistance ii) the effects of LAN on insulin resistance are reversed upon return to LD, iii) LAN exposure results in a greater increase in body weight compared to LD exposure, iv) LAN increases the incidence of mice developing overt T2DM, and v) LAN exposure decreases survival of mice with T2DM. SIGNIFICANCE: In conclusion, LAN exacerbated metabolic abnormalities in a polygenic mouse model of T2DM, and these effects were reversed upon return to dark nights. The applicability of these findings to humans with T2DM needs to be determined. |
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Department of Neuroscience, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA; Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA |
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0024-3205 |
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PMID:31207311 |
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GFZ @ kyba @ |
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2549 |
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Touitou, Y.; Reinberg, A.; Touitou, D. |
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Association between light at night, melatonin secretion, sleep deprivation, and the internal clock: Health impacts and mechanisms of circadian disruption |
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Journal Article |
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Year |
2017 |
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Life Sciences |
Abbreviated Journal |
Life Sci |
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173 |
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94-106 |
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Human Health; Review |
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Exposure to Artificial Light At Night (ALAN) results in a disruption of the circadian system, which is deleterious to health. In industrialized countries, 75% of the total workforce is estimated to have been involved in shift work and night work. Epidemiologic studies, mainly of nurses, have revealed an association between sustained night work and a 50-100% higher incidence of breast cancer. The potential and multifactorial mechanisms of the effects include the suppression of melatonin secretion by ALAN, sleep deprivation, and circadian disruption. Shift and/or night work generally decreases the time spent sleeping, and it disrupts the circadian time structure. In the long run, this desynchronization is detrimental to health, as underscored by a large number of epidemiological studies that have uncovered elevated rates of several diseases, including cancer, diabetes, cardiovascular risks, obesity, mood disorders and age-related macular degeneration. It amounts to a public health issue in the light of the very substantial number of individuals involved. The IARC has classified shift work in group 2A of “probable carcinogens to humans” since “they involve a circadian disorganization”. Countermeasures to the effects of ALAN, such as melatonin, bright light, or psychotropic drugs, have been proposed as a means to combat circadian clock disruption and improve adaptation to shift and night work. We review the evidence for the ALAN impacts on health. Furthermore, we highlight the importance of an in-depth mechanistic understanding to combat the detrimental properties of exposure to ALAN and develop strategies of prevention. |
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UHSA – Groupe Hospitalier Paul Guiraud, 54, avenue de la Republique, 94806 Villejuif, France |
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0024-3205 |
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PMID:28214594 |
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GFZ @ kyba @ |
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2455 |
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van den Heiligenberg, S.; Deprés-Brummer, P.; Barbason, H.; Claustrat, B.; Reynes, M.; Lévi, F. |
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The tumor promoting effect of constant light exposure on diethylnitrosamine-induced hepatocarcinogenesis in rats |
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1999 |
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Life Sciences |
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Life Sciences |
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64 |
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26 |
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2523-2534 |
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Human Health |
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LoNNe @ kagoburian @ |
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827 |
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