Implications of Sleep Restriction and Recovery on Metabolic Outcomes

Killick, Roo; Banks, Siobhan; Liu, Yang

doi:10.1210/jc.2012-1845

Cited by 66 publications

(75 citation statements)

References 113 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: 69%

“…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.

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: Discussionmentioning

confidence: 69%

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.

124

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“…At baseline, actigraphy showed that on average, midlife women with hot flashes slept less than the recommended amount and health consequences of disrupted and inadequate sleep are well known and of concern. [31][32][33] Future research should explore other approaches for improving sleep quality, such as cognitive behavioral therapy for insomnia, to address the important problem of sleep disturbance in women during the menopausal transition and postmenopause.…”

Section: Discussionmentioning

confidence: 99%

Effects of Yoga and Aerobic Exercise on Actigraphic Sleep Parameters in Menopausal Women with Hot Flashes

Buchanan

Landis

Hohensee

et al. 2017

Journal of Clinical Sleep Medicine

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Study Objectives: To determine effects of yoga and aerobic exercise compared with usual activity on objective assessments of sleep in midlife women. Methods: Secondary analyses of a randomized controlled trial in the Menopause Strategies: Finding Lasting Answers for Symptoms and Health (MsFLASH) network conducted among 186 late transition and postmenopausal women aged 40-62 y with hot flashes. Women were randomized to 12 w of yoga, supervised aerobic exercise, or usual activity. The mean and coefficient of variation (CV) of change in actigraph sleep measures from each intervention group were compared to the usual activity group using linear regression models. Results: Baseline values of the primary sleep measures for the entire sample were mean total sleep time (TST) = 407.5 ± 56.7 min; mean wake after sleep onset (WASO) = 54.6 ± 21.8 min; mean CV for WASO = 37.7 ± 18.7 and mean CV for number of long awakenings > 5 min = 81.5 ± 46.9. Changes in the actigraphic sleep outcomes from baseline to weeks 11-12 were small, and none differed between groups. In an exploratory analysis, women with baseline Pittsburgh Sleep Quality Index higher than 8 had significantly reduced TST-CV following yoga compared with usual activity. Conclusions: This study adds to the currently scant literature on objective sleep outcomes from yoga and aerobic exercise interventions for this population. Although small effects on self-reported sleep quality were previously reported, the interventions had no statistically significant effects on actigraph measures, except for potentially improved sleep stability with yoga in women with poor self-reported sleep quality. Keywords: actigraphy, exercise, insomnia symptoms, menopause, variability, vasomotor symptoms, yoga Citation: Buchanan DT, Landis CA, Hohensee C, Guthrie KA, Otte JL, Paudel M, Anderson GL, Caan B, Freeman EW, Joffe H, LaCroix AZ, Newton KM, Reed SD, Ensrud KE. Effects of yoga and aerobic exercise on actigraphic sleep parameters in menopausal women with hot flashes.

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“…While moderate sleep disturbance leads to stress and homeostasic imbalance (Killick et al 2012;Pellegrino et al 2012;Moller-Levet et al 2013;Gonnissen et al 2013), controlled laboratory studies in rodents have shown that prolonged sleep deprivation causes serious physiological and immunological deficits, eventually causing death (Rechtschaffen et al 1983;Bergmann et al 1989a;Everson et al 1994).…”

Section: Introductionmentioning

confidence: 99%

Sleep Deprivation and Gene Expression

Souza

Ribeiro

2015

Current Topics in Behavioral Neurosciences

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Sleep occurs in a wide range of animal species as a vital process for the maintenance of homeostasis, metabolic restoration, physiological regulation, and adaptive cognitive functions in the central nervous system. Long-term perturbations induced by the lack of sleep are mostly mediated by changes at the level of transcription and translation. This chapter reviews studies in humans, rodents, and flies to address the various ways by which sleep deprivation affects gene expression in the nervous system, with a focus on genes related to neuronal plasticity, brain function, and cognition. However, the effects of sleep deprivation on gene expression and the functional consequences of sleep loss are clearly not restricted to the cognitive domain but may include increased inflammation, expression of stress-related genes, general impairment of protein translation, metabolic imbalance, and thermal deregulation.

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Implications of Sleep Restriction and Recovery on Metabolic Outcomes

Cited by 66 publications

References 113 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

Effects of Yoga and Aerobic Exercise on Actigraphic Sleep Parameters in Menopausal Women with Hot Flashes

Sleep Deprivation and Gene Expression

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