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Eisenstein, M. (2013). Chronobiology: stepping out of time. Nature, 497(7450), S10–2.
Keywords: Human Health; Animals; Benzofurans/therapeutic use; CLOCK Proteins/genetics/metabolism; Circadian Rhythm/genetics/*physiology; Cyclopropanes/therapeutic use; Efficiency/physiology; Humans; Melatonin/agonists/metabolism; Obesity/metabolism; Sleep/genetics/*physiology; Suprachiasmatic Nucleus/metabolism
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Fonken, L. K., Aubrecht, T. G., Melendez-Fernandez, O. H., Weil, Z. M., & Nelson, R. J. (2013). Dim light at night disrupts molecular circadian rhythms and increases body weight. J Biol Rhythms, 28(4), 262–271.
Abstract: With the exception of high latitudes, life has evolved under bright days and dark nights. Most organisms have developed endogenously driven circadian rhythms that are synchronized to this daily light/dark cycle. In recent years, humans have shifted away from the naturally occurring solar light cycle in favor of artificial and sometimes irregular light schedules produced by electric lighting. Exposure to unnatural light cycles is increasingly associated with obesity and metabolic syndrome; however, the means by which environmental lighting alters metabolism are poorly understood. Thus, we exposed mice to dim light at night and investigated changes in the circadian system and metabolism. Here we report that exposure to ecologically relevant levels of dim (5 lux) light at night altered core circadian clock rhythms in the hypothalamus at both the gene and protein level. Circadian rhythms in clock expression persisted during light at night; however, the amplitude of Per1 and Per2 rhythms was attenuated in the hypothalamus. Circadian oscillations were also altered in peripheral tissues critical for metabolic regulation. Exposure to dimly illuminated, as compared to dark, nights decreased the rhythmic expression in all but one of the core circadian clock genes assessed in the liver. Additionally, mice exposed to dim light at night attenuated Rev-Erb expression in the liver and adipose tissue. Changes in the circadian clock were associated with temporal alterations in feeding behavior and increased weight gain. These results are significant because they provide evidence that mild changes in environmental lighting can alter circadian and metabolic function. Detailed analysis of temporal changes induced by nighttime light exposure may provide insight into the onset and progression of obesity and metabolic syndrome, as well as other disorders involving sleep and circadian rhythm disruption.
Keywords: Animals; Blood Glucose/metabolism; Body Weight/*physiology; CLOCK Proteins/biosynthesis/genetics; Circadian Rhythm/*physiology; Corticosterone/metabolism; Feeding Behavior/physiology; Immunohistochemistry; Light; *Lighting; Male; Mice; Motor Activity; Polymerase Chain Reaction; Suprachiasmatic Nucleus/metabolism/physiology; clock genes; feeding rhythm; light pollution; obesity
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Garaulet, M., Ordovas, J. M., & Madrid, J. A. (2010). The chronobiology, etiology and pathophysiology of obesity. Int J Obes (Lond), 34(12), 1667–1683.
Abstract: The effect of CD on human health is an emerging issue. Many records link CD with diseases such as cancer, cardiovascular, cognitive impairment and obesity, all of them conducive to premature aging. The amount of sleep has declined by 1.5 h over the past century, accompanied by an important increase in obesity. Shift work, sleep deprivation and exposure to bright light at night increase the prevalence of adiposity. Animal models have shown that mice with Clock gene disruption are prone to developing obesity and MetS. This review summarizes the latest developments with regard to chronobiology and obesity, considering (1) how molecular clocks coordinate metabolism and the specific role of the adipocyte; (2) CD and its causes and pathological consequences; (3) the epidemiological evidence of obesity as a chronobiological illness; and (4) theories of circadian disruption and obesity. Energy intake and expenditure, relevance of sleep, fat intake from a circadian perspective and psychological and genetic aspects of obesity are examined. Finally, ideas about the use of chronobiology in the treatment of obesity are discussed. Such knowledge has the potential to become a valuable tool in the understanding of the relationship between the chronobiology, etiology and pathophysiology of obesity.
Keywords: Human Health; Animals; CLOCK Proteins/genetics/*physiology; Circadian Rhythm/genetics/*physiology; Energy Intake/*physiology; Feeding Behavior/physiology; Humans; Mice; Motor Activity/physiology; *Obesity/etiology/physiopathology; Sleep/physiology; Sleep Deprivation/complications/genetics/*physiopathology
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Kempinger, L., Dittmann, R., Rieger, D., & Helfrich-Forster, C. (2009). The nocturnal activity of fruit flies exposed to artificial moonlight is partly caused by direct light effects on the activity level that bypass the endogenous clock. Chronobiol Int, 26(2), 151–166.
Abstract: Artificial moonlight was recently shown to shift the endogenous clock of fruit flies and make them nocturnal. To test whether this nocturnal activity is partly due to masking effects of light, we exposed the clock-mutants per(01), tim(01), per(01);tim(01), cyc(01), and Clk(JRK) to light/dark and light/dim-light cycles and determined the activity level during the day and night. We found that under moonlit nights, all clock mutants shifted their activity significantly into the night, suggesting that this effect is independent of the clock. We also recorded the flies under continuous artificial moonlight and darkness to judge the effect of dim constant light on the activity level. All mutants, except Clk(JRK) flies, were significantly more active under artificial moonlight conditions than under complete darkness. Unexpectedly, we found residual rhythmicity of per(01) and especially tim(01) mutants under these conditions, suggesting that TIM and especially PER retained some activity in the absence of its respective partner. Nevertheless, as even the double mutants and the cyc(01) and Clk(JRK) mutants shifted their activity into the night, we conclude that dim light stimulates the activity of fruit flies in a clock-independent manner. Thus, nocturnal light has a twofold influence on flies: it shifts the circadian clock, and it increases nocturnal activity independently of the clock. The latter was also observed in some primates by others and might therefore be of a more general validity.
Keywords: ARNTL Transcription Factors; Animals; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism; Behavior, Animal/physiology; Biological Clocks/*physiology; CLOCK Proteins; Circadian Rhythm/*physiology; Darkness; Drosophila Proteins/genetics/metabolism; Drosophila melanogaster/*physiology; *Light; *Moon; Motor Activity/*physiology; Nuclear Proteins/genetics/metabolism; Period Circadian Proteins; Photoperiod; Transcription Factors/genetics/metabolism
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Kovac, J., Husse, J., & Oster, H. (2009). A time to fast, a time to feast: the crosstalk between metabolism and the circadian clock. Mol Cells, 28(2), 75–80.
Abstract: The cyclic environmental conditions brought about by the 24 h rotation of the earth have allowed the evolution of endogenous circadian clocks that control the temporal alignment of behaviour and physiology, including the uptake and processing of nutrients. Both metabolic and circadian regulatory systems are built upon a complex feedback network connecting centres of the central nervous system and different peripheral tissues. Emerging evidence suggests that circadian clock function is closely linked to metabolic homeostasis and that rhythm disruption can contribute to the development of metabolic disease. At the same time, metabolic processes feed back into the circadian clock, affecting clock gene expression and timing of behaviour. In this review, we summarize the experimental evidence for this bimodal interaction, with a focus on the molecular mechanisms mediating this exchange, and outline the implications for clock-based and metabolic diseases.
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