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Author Russart, K.L.G.; Chbeir, S.A.; Nelson, R.J.; Magalang, U.J.
Title Light at night exacerbates metabolic dysfunction in a polygenic mouse model of type 2 diabetes mellitus Type Journal Article
Year 2019 Publication Life Sciences Abbreviated Journal Life Sci
Volume 231 Issue Pages 116574
Keywords Animals; diabetes; human health; mouse models; Type 2 diabetes; Insulin Resistance
Abstract (up) 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.
Address 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
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 0024-3205 ISBN Medium
Area Expedition Conference
Notes PMID:31207311 Approved no
Call Number GFZ @ kyba @ Serial 2549
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Author Qian, J.; Scheer, F.A.J.L.
Title Circadian System and Glucose Metabolism: Implications for Physiology and Disease Type Journal Article
Year 2016 Publication Trends in Endocrinology and Metabolism: TEM Abbreviated Journal Trends Endocrinol Metab
Volume 27 Issue 5 Pages 282-293
Keywords Human Health; circadian rhythms; food timing; glucose metabolism; melatonin; sleep; type 2 diabetes
Abstract (up) The circadian system serves one of the most fundamental properties present in nearly all organisms: it generates 24-h rhythms in behavioral and physiological processes and enables anticipating and adapting to daily environmental changes. Recent studies indicate that the circadian system is important in regulating the daily rhythm in glucose metabolism. Disturbance of this circadian control or of its coordination relative to the environmental/behavioral cycle, such as in shift work, eating late, or due to genetic changes, results in disturbed glucose control and increased type 2 diabetes risk. Therefore, an in-depth understanding of the mechanisms underlying glucose regulation by the circadian system and its disturbance may help in the development of therapeutic interventions against the deleterious health consequences of circadian disruption.
Address Medical Chronobiology Program, Division of Sleep and Circadian Disorders, Brigham and Women's Hospital, Boston, MA 02115, USA; Division of Sleep Medicine, Harvard Medical School, Boston, MA 02115, USA; fscheer(at)bwh.harvard.edu
Corporate Author Thesis
Publisher Cell Place of Publication Editor
Language English Summary Language English Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1043-2760 ISBN Medium
Area Expedition Conference
Notes PMID:27079518; PMCID:PMC4842150 Approved no
Call Number IDA @ john @ Serial 1446
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Author Rakshit, K.; Thomas, A.P.; Matveyenko, A.V.
Title Does disruption of circadian rhythms contribute to beta-cell failure in type 2 diabetes? Type Journal Article
Year 2014 Publication Current Diabetes Reports Abbreviated Journal Curr Diab Rep
Volume 14 Issue 4 Pages 474
Keywords *epidemiology; diabetes; Type 2 diabetes; beta cell; T2DM; artificial light; light exposure; circadian disruption
Abstract (up) Type 2 diabetes mellitus (T2DM) is a complex metabolic disease characterized by the loss of beta-cell secretory function and mass. The pathophysiology of beta-cell failure in T2DM involves a complex interaction between genetic susceptibilities and environmental risk factors. One environmental condition that is gaining greater appreciation as a risk factor for T2DM is the disruption of circadian rhythms (eg, shift-work and sleep loss). In recent years, circadian disruption has become increasingly prevalent in modern societies and consistently shown to augment T2DM susceptibility (partly mediated through its effects on pancreatic beta-cells). Since beta-cell failure is essential for development of T2DM, we will review current work from epidemiologic, clinical, and animal studies designed to gain insights into the molecular and physiological mechanisms underlying the predisposition to beta-cell failure associated with circadian disruption. Elucidating the role of circadian clocks in regulating beta-cell health will add to our understanding of T2DM pathophysiology and may contribute to the development of novel therapeutic and preventative approaches.
Address Larry L. Hillblom Islet Research Center, Department of Medicine, Division of Endocrinology, University of California Los Angeles, David Geffen School of Medicine, Los Angeles, California, 900A Weyburn Place, Los Angeles, CA, 90095, USA
Corporate Author Thesis
Publisher Springer Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1534-4827 ISBN Medium
Area Expedition Conference
Notes PMID:24532160; PMCID:PMC3988110 Approved no
Call Number IDA @ john @ Serial 320
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