Dim Light at Night Disrupts Molecular Circadian Rhythms and Increases Body Weight

Fonken, Laura K.; Aubrecht, Taryn G.; Meléndez-Fernández, O. Hecmarie; Weil, Zachary M.

doi:10.1177/0748730413493862

Cited by 248 publications

(205 citation statements)

References 47 publications

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“…Interestingly, the amplitude of electrical activity in the SCN is linked to sympathetic outflow toward multiple organs (25). This mechanism also explains previous findings that exposure of mice to dim light (5 lx) during 10-h nights for 4 wk already results in an increase in body weight, which was accompanied by an attenuated amplitude of circadian gene expression in the hypothalamus (26). Additionally, sympathetic outflow toward BAT depots other than interscapular BAT = not significant, *P < 0.05, **P < 0.01, ***P < 0.001.…”

Section: Discussionsupporting

confidence: 72%

Prolonged daily light exposure increases body fat mass through attenuation of brown adipose tissue activity

Kooijman¹,

Berg²,

Ramkisoensing

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

124

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Disruption of circadian rhythmicity is associated with obesity and related disorders, including type 2 diabetes and cardiovascular disease. Specifically, prolonged artificial light exposure associates with obesity in humans, although the underlying mechanism is unclear. Here, we report that increasing the daily hours of light exposure increases body adiposity through attenuation of brown adipose tissue (BAT) activity, a major contributor of energy expenditure. Mice exposed to a prolonged day length of 16-and 24-h light, compared with regular 12-h light, showed increased adiposity without affecting food intake or locomotor activity. Mechanistically, we demonstrated that prolonged day length decreases sympathetic input into BAT and reduces β3-adrenergic intracellular signaling. Concomitantly, prolonging day length decreased the uptake of fatty acids from triglyceride-rich lipoproteins, as well as of glucose from plasma selectively by BAT. We conclude that impaired BAT activity is an important mediator in the association between disturbed circadian rhythm and adiposity, and anticipate that activation of BAT may overcome the adverse metabolic consequences of disturbed circadian rhythmicity. M odern world society is subjected to disturbances of circadian rhythms by shift work, sleep deprivation, and environmental light pollution. Importantly, the increasing prevalence of obesity is associated with a disrupted sleep-wake pattern in humans (1) and coincides with the availability of artificial light (2, 3). Additionally, a recent study revealed a relationship between exposure to light at night and obesity in a cross-sectional analysis of over 100,000 women (4). Light input is the most important cue for generation of circadian (∼24 h) rhythms by the master clock. Both in rodents and humans the master clock is situated in the suprachiasmatic nucleus (SCN) of the hypothalamus. The SCN is responsible for synchronization of peripheral clocks throughout the body, which is mediated by endocrine and neuronal signals (5). A causal role for a disturbed circadian rhythm in the development of obesity has been demonstrated by animal studies. Mice with genetically dysfunctional clock genes develop obesity and insulin resistance (6-9). Moreover, specific ablation of the SCN induces acute weight gain (10). These results indicate a crucial role for the SCN in the regulation of adiposity.Interestingly, we previously showed that prolonged light exposure only is sufficient to enhance weight gain in mice. Constant light disrupts the central circadian clock, evidenced by an immediate reduction in the circadian amplitude of SCN electrical activity. Moreover, constant light induces body weight gain and insulin resistance, even faster than high-fat diet, which was not caused by increased food intake or reduced locomotor activity (11). Therefore, disruption of the central biological clock likely induces weight gain by decreasing energy expenditure.Recently, it has been recognized that brown adipose tissue (BAT) importantly contributes to energy ...

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Section: Discussionsupporting

confidence: 72%

Prolonged daily light exposure increases body fat mass through attenuation of brown adipose tissue activity

Kooijman¹,

Berg²,

Ramkisoensing

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

124

View full text Add to dashboard Cite

show abstract

“…For instance, as the expression of the negative clock gene Per is normally low at night, light administered during the subjective night should significantly alter the pattern of Per expression and consequently affect other components of the circadian clock. Dim light at night (~5 lux) has been shown to alter circadian clock gene expression of mice (Fonken et al 2013a ; Fonken andNelson 2014 ) and Siberian hamsters (Bedrosian et al 2013 ), including Bmal1, Per1, Per2, Cry1, Cry2, and Rev Erb. These effects have been reported in both the SCN and the liver, with the latter associated with increased body weight independently of daily caloric intake (Fonken et al 2013a ).…”

Section: Future Directionsmentioning

confidence: 99%

The effects of light pollution on biological rhythms of birds: an integrated, mechanistic perspective

Dominoni

2015

J Ornithol

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Light pollution is considered a threat for biodiversity given the extent to which it can affect a vast number of behavioral and physiological processes in several species. This comes as no surprise as light is a fundamental, environmental cue through which organisms time their daily and seasonal activities, and alterations in the light environment have been found to affect profoundly the synchronization of the circadian clock, the endogenous mechanism that tracks and predicts variation in the external light/dark cycles. In this context, birds have been one of the most studied animal taxa, but our understanding of the effects of light pollution on the biological rhythms of avian species is mostly limited to behavioral responses. In order to understand which proximate mechanisms may be affected by artificial lights, we need an integrated perspective that focuses on light as a physiological signal, and especially on how photic information is perceived, decoded, and transmitted through the whole body. The aim of this review is to summarize the effects of light pollution on physiological and biochemical mechanisms that underlie changes in birds' behavior, highlighting the current gaps in our knowledge and proposing future research avenues.

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“…MLT treatment consistently reduced adiposity and body mass in several rodent species [182]. Several studies have demonstrated that chronic exposure to dim light at night increases body mas gain in mice, and this effect is suggested to be mediated by the ALAN-induced MLT suppression [91,92,191,192]. Finally, MLT has been reported to influence several metabolic factors, such as insulin, insulin-like growth factor, growth hormone, glucose metabolism, and others, which could directly control body mass homeostasis [193].…”

Section: Alan Obesity and Cancerthe Epigenetic Nexus To Melatoninmentioning

confidence: 97%

“…ALAN treatments result in a significant reduction in daily energy expenditure and body mass of social voles (Microtus socialis) and laboratory rats [89,90]. In another mice experiment, circadian disruption by dim florescent ALAN has been reported to change feeding behavior and increased mass gain [91,92]. This contrasting effect of ALAN on body mass could be at least partially explained by the different light intensity levels used in the comparative studies; where the direction of body mass change can be directly related to light intensity levels.…”

Section: Lan and Circadian Disruption Of Metabolic Responsesmentioning

confidence: 98%

Artificial light-at-night – a novel lifestyle risk factor for metabolic disorder and cancer morbidity

Zubidat

Haim

2017

Journal of Basic and Clinical Physiology and Pharmacology

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Both obesity and breast cancer are already recognized worldwide as the most common syndromes in our modern society. Currently, there is accumulating evidence from epidemiological and experimental studies suggesting that these syndromes are closely associated with circadian disruption. It has been suggested that melatonin (MLT) and the circadian clock genes both play an important role in the development of these syndromes. However, we still poorly understand the molecular mechanism underlying the association between circadian disruption and the modern health syndromes. One promising candidate is epigenetic modifications of various genes, including clock genes, circadian-related genes, oncogenes, and metabolic genes. DNA methylation is the most prominent epigenetic signaling tool for gene expression regulation induced by environmental exposures, such as artificial light-at-night (ALAN). In this review, we first provide an overview on the molecular feedback loops that generate the circadian regulation and how circadian disruption by ALAN can impose adverse impacts on public health, particularly metabolic disorders and breast cancer development. We then focus on the relation between ALAN-induced circadian disruption and both global DNA methylation and specific loci methylation in relation to obesity and breast cancer morbidities. DNA hypo-methylation and DNA hyper-methylation, are suggested as the most studied epigenetic tools for the activation and silencing of genes that regulate metabolic and monostatic responses. Finally, we discuss the potential clinical and therapeutic roles of MLT suppression and DNA methylation patterns as novel biomarkers for the early detection of metabolic disorders and breast cancer development.

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Dim Light at Night Disrupts Molecular Circadian Rhythms and Increases Body Weight

Cited by 248 publications

References 47 publications

Prolonged daily light exposure increases body fat mass through attenuation of brown adipose tissue activity

Prolonged daily light exposure increases body fat mass through attenuation of brown adipose tissue activity

The effects of light pollution on biological rhythms of birds: an integrated, mechanistic perspective

Artificial light-at-night – a novel lifestyle risk factor for metabolic disorder and cancer morbidity

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