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Buijs, F. N., Leon-Mercado, L., Guzman-Ruiz, M., Guerrero-Vargas, N. N., Romo-Nava, F., & Buijs, R. M. (2016). The Circadian System: A Regulatory Feedback Network of Periphery and Brain. Physiology (Bethesda), 31(3), 170–181.
Abstract: Circadian rhythms are generated by the autonomous circadian clock, the suprachiasmatic nucleus (SCN), and clock genes that are present in all tissues. The SCN times these peripheral clocks, as well as behavioral and physiological processes. Recent studies show that frequent violations of conditions set by our biological clock, such as shift work, jet lag, sleep deprivation, or simply eating at the wrong time of the day, may have deleterious effects on health. This infringement, also known as circadian desynchronization, is associated with chronic diseases like diabetes, hypertension, cancer, and psychiatric disorders. In this review, we will evaluate evidence that these diseases stem from the need of the SCN for peripheral feedback to fine-tune its output and adjust physiological processes to the requirements of the moment. This feedback can vary from neuronal or hormonal signals from the liver to changes in blood pressure. Desynchronization renders the circadian network dysfunctional, resulting in a breakdown of many functions driven by the SCN, disrupting core clock rhythms in the periphery and disorganizing cellular processes that are normally driven by the synchrony between behavior and peripheral signals with neuronal and humoral output of the hypothalamus. Consequently, we propose that the loss of synchrony between the different elements of this circadian network as may occur during shiftwork and jet lag is the reason for the occurrence of health problems.
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Fonken, L. K., & Nelson, R. J. (2014). The Effects of Light at Night on Circadian Clocks and Metabolism. In Endocrine Reviews (Vol. 35, pp. 648–670). Endocrine Society.
Abstract: Most organisms display endogenously produced approximately ~24 h fluctuations in physiology and behavior, termed circadian rhythms. Circadian rhythms are driven by a transcriptional-translational feedback loop that is hierarchically expressed throughout the brain and body, with the suprachiasmatic nucleus of the hypothalamus serving as the master circadian oscillator at the top of the hierarchy. Appropriate circadian regulation is important for many homeostatic functions including energy regulation. Multiple genes involved in nutrient metabolism display rhythmic oscillations and metabolically related hormones such as glucagon, insulin, ghrelin, leptin, and corticosterone are released in a circadian fashion. Mice harboring mutations in circadian clock genes alter feeding behavior, endocrine signaling, and dietary fat absorption. Moreover, misalignment between behavioral and molecular circadian clocks can result in obesity in both rodents and humans. Importantly, circadian rhythms are most potently synchronized to the external environment by light information and exposure to light at night potentially disrupts circadian system function. Since the advent of electric lights around the turn of the 20th century, exposure to artificial and irregular light schedules has become commonplace. The increase in exposure to light at night parallels the global increase in the prevalence of obesity and metabolic disorders. In this review, we propose that exposure to light at night alters metabolic function through disruption of the circadian system. We first provide an introduction to the circadian system, with a specific emphasis on the effects of light on circadian rhythms. Next we address interactions between the circadian system and metabolism. Finally, we review current experimental and epidemiological work directly associating exposure to light at night and metabolism.
Keywords: *Circadian Rhythm; clock genes; *epidemiology; light at night; review
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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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Kavcic, P., Rojc, B., Dolenc-Groselj, L., Claustrat, B., Fujs, K., & Poljak, M. (2011). The impact of sleep deprivation and nighttime light exposure on clock gene expression in humans. Croat Med J, 52(5), 594–603.
Abstract: Aim
To examine the effect of acute sleep deprivation under light conditions on the expression of two key clock genes, hPer2 and hBmal1, in peripheral blood mononuclear cells (PBMC) and on plasma melatonin and cortisol levels. Methods Blood samples were drawn from 6 healthy individuals at 4-hour intervals for three consecutive nights, including a night of total sleep deprivation (second night). The study was conducted in April-June 2006 at the University Medical Centre Ljubljana. Results We found a significant diurnal variation in hPer2 and hBmal1 expression levels under baseline (P < 0.001, F = 19.7, df = 30 for hPer2 and P < 0.001, F = 17.6, df = 30 for hBmal1) and sleep-deprived conditions (P < 0.001, F = 9.2, df = 30 for hPer2 and P < 0.001, F = 13.2, df = 30 for hBmal1). Statistical analysis with the single cosinor method revealed circadian variation of hPer2 under baseline and of hBmal1 under baseline and sleep-deprived conditions. The peak expression of hPer2 was at 13:55 ± 1:15 hours under baseline conditions and of hBmal1 at 16:08 ± 1:18 hours under baseline and at 17:13 ± 1:35 hours under sleep-deprived conditions. Individual cosinor analysis of hPer2 revealed a loss of circadian rhythm in 3 participants and a phase shift in 2 participants under sleep-deprived conditions. The plasma melatonin and cortisol rhythms confirmed a conventional alignment of the central circadian pacemaker to the habitual sleep/wake schedule. Conclusion Our results suggest that 40-hour acute sleep deprivation under light conditions may affect the expression of hPer2 in PBMCs. Keywords: genomics; epigenetics; hPer2; hBmal1; clock genes; gene expression; biology; human health
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Oike, H., Sakurai, M., Ippoushi, K., & Kobori, M. (2015). Time-fixed feeding prevents obesity induced by chronic advances of light/dark cycles in mouse models of jet-lag/shift work. Biochem Biophys Res Commun, 465(3), 556–561.
Abstract: Recent findings have uncovered intimate relationships between circadian clocks and energy metabolism. Epidemiological studies have shown that the frequency of obesity and metabolic disorders increases among shift-workers. Here we found that a chronic shift in light/dark (LD) cycles comprising an advance of six hours twice weekly, induced obesity in mice. Under such conditions that imitate jet lag/shift work, body weight and glucose intolerance increased, more fat accumulated in white adipose tissues and the expression profiles of metabolic genes changed in the liver compared with normal LD conditions. Mice fed at a fixed 12 h under the LD shift notably did not develop symptoms of obesity despite isocaloric intake. These results suggest that jet lag/shift work induces obesity as a result of fluctuating feeding times and it can be prevented by fixing meal times. This rodent model of obesity might serve as a useful tool for understanding why shift work induces metabolic disorders.
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