Exposure to Light at Night, Nocturnal Urinary Melatonin Excretion, and Obesity/Dyslipidemia in the Elderly: A Cross-Sectional Analysis of the HEIJO-KYO Study

Obayashi, Kenji; Saeki, Keigo; Iwamoto, Junko; Okamoto, Nobuhiko; Tomioka, Kimiko; Nezu, Satoko; Ikada, Yoshito; Kurumatani, Norio

doi:10.1210/jc.2012-2874

Cited by 156 publications

(127 citation statements)

References 42 publications

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“…Based on our present data, the daily light exposure may thus well explain the circannual cycle of BAT detectability. Similarly, impaired BAT activity may also explain, at least partly, the relationship between obesity and disturbances in circadian rhythmicity in humans by light pollution (2,3,34), and possibly also by shift work (35)(36)(37) and sleep curtailment (1,38,39). Additionally, our data may provide the link in the relationship between exposure to light in the bedroom and obesity (4).…”

Section: Discussionmentioning

confidence: 67%

“…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).…”

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confidence: 99%

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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.

121

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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: Discussionmentioning

confidence: 67%

mentioning

confidence: 99%

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.

121

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“…In the home setting, bedroom light intensity had a positive correlation with the prevalence of obesity (109,110) and evening artificial light intensity showed a positive correlation with the incidence of type 2 diabetes (111) . Furthermore, daytime light exposure was positively correlated with BMI (112) .…”

Section: Effect Of Light On Food Intake Body Weight and Glucose Metamentioning

confidence: 99%

Nutrition in the spotlight: metabolic effects of environmental light

et al. 2016

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Use of artificial light resulted in relative independence from the natural light-dark (LD) cycle, allowing human subjects to shift the timing of food intake and work to convenient times. However, the increase in artificial light exposure parallels the increase in obesity prevalence. Light is the dominant Zeitgeber for the central circadian clock, which resides within the hypothalamic suprachiasmatic nucleus, and coordinates daily rhythm in feeding behaviour and metabolism. Eating during inappropriate light conditions may result in metabolic disease via changes in the biological clock. In this review, we describe the physiological role of light in the circadian timing system and explore the interaction between the circadian timing system and metabolism. Furthermore, we discuss the acute and chronic effects of artificial light exposure on food intake and energy metabolism in animals and human subjects. We propose that living in synchrony with the natural daily LD cycle promotes metabolic health and increased exposure to artificial light at inappropriate times of day has adverse effects on metabolism, feeding behaviour and body weight regulation. Reducing the negative side effects of the extensive use of artificial light in human subjects might be useful in the prevention of metabolic disease.Artificial light: Circadian: Glucose metabolism: Obesity Changes in artificial light exposureObesity is an increasing health problem and is associated with the development of type 2 diabetes and CVD (1) . The pathophysiology of obesity is multifactorial, with the major contributions from overconsumption of highenergy highly palatable food and an inactive lifestyle (2) . One modern environmental factor that contributes to changes in eating behaviour is the widespread use of artificial light. The relative independence from the natural light-dark (LD) cycle, allows people to eat and engage in activities until late in the evening and at night. Artificial light has also led to an increase in nighttime sky glow and to the transformation of nightscapes. More than 99% of the US and EU population, and about two-thirds of the world population lives in areas where the night sky is illuminated above the threshold for light pollution (artificial sky brightness greater than 10% of the natural night sky brightness above 45°eleva-tion). Moreover, satellite data show that 70% of the US population and 50% of the European population can no longer see the Milky Way, even under the best conditions (3) . Cinzano et al. (3) calculated that only 40% of Americans live in a location where it becomes sufficiently dark at night for the human eye to make a complete transition from cone to rod vision. Despite the benefits for

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“…These include light at night (37,68), study-associated stress or interindividual differences in basal stress levels or stress tolerability (e.g., via effects on cortisol and sympathetic activity) (18,69), lifestyle factors of the participants, sedentary versus mobile state (9), and ambient temperature (70). As an example, environmental temperature can affect energy expenditure under both sedentary and active conditions (71).…”

Section: Experimental and Environmental Conditionsmentioning

confidence: 99%

Determinants of Shortened, Disrupted, and Mistimed Sleep and Associated Metabolic Health Consequences in Healthy Humans

2015

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Recent increases in the prevalence of obesity and type 2 diabetes mellitus (T2DM) in modern societies have been paralleled by reductions in the time their denizens spend asleep. Epidemiological studies have shown that disturbed sleep—comprising short, low-quality, and mistimed sleep—increases the risk of metabolic diseases, especially obesity and T2DM. Supporting a causal role of disturbed sleep, experimental animal and human studies have found that sleep loss can impair metabolic control and body weight regulation. Possible mechanisms for the observed changes comprise sleep loss–induced changes in appetite-signaling hormones (e.g., higher levels of the hunger-promoting hormone ghrelin) or hedonic brain responses, altered responses of peripheral tissues to metabolic signals, and changes in energy intake and expenditure. Even though the overall consensus is that sleep loss leads to metabolic perturbations promoting the development of obesity and T2DM, experimental evidence supporting the validity of this view has been inconsistent. This Perspective aims at discussing molecular to behavioral factors through which short, low-quality, and mistimed sleep may threaten metabolic public health. In this context, possible factors that may determine the extent to which poor sleep patterns increase the risk of metabolic pathologies within and across generations will be discussed (e.g., timing and genetics).

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Exposure to Light at Night, Nocturnal Urinary Melatonin Excretion, and Obesity/Dyslipidemia in the Elderly: A Cross-Sectional Analysis of the HEIJO-KYO Study

Cited by 156 publications

References 42 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

Nutrition in the spotlight: metabolic effects of environmental light

Determinants of Shortened, Disrupted, and Mistimed Sleep and Associated Metabolic Health Consequences in Healthy Humans

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