Time-fixed feeding prevents obesity induced by chronic advances of light/dark cycles in mouse models of jet-lag/shift work

Oike, Hideaki; Sakurai, Mutsumi; Ippoushi, Katsunari; Kobori, Masuko

doi:10.1016/j.bbrc.2015.08.059

Cited by 61 publications

(45 citation statements)

References 29 publications

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“…In the present experiments, chronic 12‐h advances in the LD cycle were observed to disrupt photic entrainment of circadian behavior, modulate clock gene rhythms in the spleen and adipose tissue macrophages, and similarly exacerbate HFD‐induced increases in body weight, glucose intolerance, and insulin resistance. Consistent with other rodent studies examining the effects of various chronic jet lag or shift work paradigms on diet‐induced metabolic pathophysiology (28, 29), these findings suggest that environmental alteration or modulation of circadian rhythms is sufficient to disrupt metabolic homeostasis. Interestingly, the observed effects of shifted LD cycles on metabolism were not accompanied by a corresponding increase in total daily food intake.…”

Section: Discussionsupporting

confidence: 86%

Shift work cycle‐induced alterations of circadian rhythms potentiate the effects of high‐fat diet on inflammation and metabolism

et al. 2018

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Based on genetic models with mutation or deletion of core clock genes, circadian disruption has been implicated in the pathophysiology of metabolic disorders. Thus, we examined whether circadian desynchronization in response to shift work-type schedules is sufficient to compromise metabolic homeostasis and whether inflammatory mediators provide a key link in the mechanism by which alterations of circadian timekeeping contribute to diet-induced metabolic dysregulation. In high-fat diet (HFD)-fed mice, exposure to chronic shifts of the light-dark cycle (12 h advance every 5 d): 1) disrupts photoentrainment of circadian behavior and modulates the period of spleen and macrophage clock gene rhythms; 2) potentiates HFD-induced adipose tissue infiltration and activation of proinflammatory M1 macrophages; 3) amplifies macrophage proinflammatory cytokine expression in adipose tissue and bone marrow-derived macrophages; and 4) exacerbates diet-induced increases in body weight, insulin resistance, and glucose intolerance in the absence of changes in total daily food intake. Thus, complete disruption of circadian rhythmicity or clock gene function as transcription factors is not requisite to the link between circadian and metabolic phenotypes. These findings suggest that macrophage proinflammatory activation and inflammatory signaling are key processes in the physiologic cascade by which dysregulation of circadian rhythmicity exacerbates diet-induced systemic insulin resistance and glucose intolerance.-Kim, S.-M., Neuendorff, N., Alaniz, R. C., Sun, Y., Chapkin, R. S., Earnest, D. J. Shift work cycle-induced alterations of circadian rhythms potentiate the effects of high-fat diet on inflammation and metabolism.

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Section: Discussionsupporting

confidence: 86%

Shift work cycle‐induced alterations of circadian rhythms potentiate the effects of high‐fat diet on inflammation and metabolism

et al. 2018

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“…In contrast, restricting feeding to a fixed 12-hour window protected jetlagged animals from the induction of obesity, despite isocaloric intake [23]*. Interestingly, the 12 hours of fixed feeding did not systematically occur during the active phase, but consisted of a set 12-hour window that did not shift when the mice were advanced, which resulted in the food availability window occurring during the light phase in some parts of the protocol, and during the dark phase at others.…”

Section: Introductionmentioning

confidence: 99%

Disturbances of sleep and circadian rhythms: novel risk factors for obesity

Broussard

Cauter²

2016

Current Opinion in Endocrinology, Diabetes &Amp; Obesity

152

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Purpose of review To summarize recent developments linking disturbances of sleep and circadian rhythms to an increased risk for obesity, and to review novel research on potential countermeasures. Recent findings Effective treatments for obesity are limited, with long-term adherence to life style changes proving difficult. Identifying new preventive strategies based on modifiable risk factors is therefore imperative in the fight against obesity. Disturbances of sleep and circadian rhythms have an adverse impact on food choices, hunger and appetite and have lifelong deleterious metabolic effects when present during childhood and early adulthood. The upregulation of the endocannabinoid system and abnormalities in the temporal distribution of caloric intake have been recently implicated in the link between sleep loss and obesity risk. Lastly, alterations in the circadian variation in the composition and functionality of the gut microbiome have been identified as potential contributors to metabolic dysfunction in conditions of jet lag and shift work. Insufficient sleep and circadian misalignment are thus new modifiable risk factors for obesity. Emerging evidence suggests that novel countermeasures, such as manipulations of the timing of food intake, may be effective strategies in the prevention of obesity. Summary Four important findings are briefly reviewed: 1. disturbances of sleep and circadian rhythms in children and young adults are risk factors for the development of lifelong obesity; 2. circadian misalignment, as occurs in shift work, has an adverse impact on energy balance and increases the risk of weight gain; 3. the endocannabinoid system, an important regulator of hedonic feeding, could be a potential link between sleep, circadian rhythms and feeding behavior; 4. disturbances of the circadian variation in composition of the gut microbiome could be involved in the increased risk of obesity associated with insufficient sleep and circadian misalignment.

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“…55 If clock disturbances become chronic, such as in rotating shift work regimes, inner clocks cannot adapt anymore and severe metabolic consequences can result, as seen in mice that were repeatedly exposed to 6 hours per day advances in the light/dark cycle and gained more weight than their nonshifted littermates. 56 Interestingly some animal sleep restriction or shift work studies yield contradictory results and increased weight gain was not always observed in the challenged animals. 57,58 An important factor appears to be whether the sleep/shift paradigm also triggers mistimed food intake.…”

Section: Peripher Al and Centr Al Interpl Ay In Homeos Tati C And Cmentioning

confidence: 99%

“…57,58 An important factor appears to be whether the sleep/shift paradigm also triggers mistimed food intake. 56,59 Food is a strong timing signal for peripheral tissue clocks. 60 Food consumption during the normal rest hours is not only a direct resetting cue for peripheral clocks, but also may have clock-independent metabolic and weight effects.…”

Section: Peripher Al and Centr Al Interpl Ay In Homeos Tati C And Cmentioning

confidence: 99%

Interplay of central and peripheral circadian clocks in energy metabolism regulation

Kolbe

Brehm

Oster

2018

J Neuroendocrinology

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Metabolic health founds on a homeostatic balance that has to integrate the daily changes of rest/activity and feeding/fasting cycles. A network of endogenous 24‐hour circadian clocks helps to anticipate daily recurring events and adjust physiology and behavioural functions accordingly. Circadian clocks are self‐sustained cellular oscillators based on a set of clock genes/proteins organised in interlocked transcriptional‐translational feedback loops. The body's clocks need to be regularly reset and synchronised with each other to achieve coherent rhythmic output signals. This synchronisation is achieved by interplay of a master clock, which resides in the suprachiasmatic nucleus, and peripheral tissue clocks. This clock network is reset by time signals such as the light/dark cycle, food intake and activity. The balanced interplay of clocks is easily disturbed in modern society by shiftwork or high‐energy diets, which may further promote the development of metabolic disorders. In this review, we summarise the current model of central‐peripheral clock interaction in metabolic health. Different established mouse models for central or peripheral clock disruption and their metabolic phenotypes are compared and the possible relevance of clock network interaction for the development of therapeutic approaches in humans is discussed.

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Time-fixed feeding prevents obesity induced by chronic advances of light/dark cycles in mouse models of jet-lag/shift work

Cited by 61 publications

References 29 publications

Shift work cycle‐induced alterations of circadian rhythms potentiate the effects of high‐fat diet on inflammation and metabolism

Shift work cycle‐induced alterations of circadian rhythms potentiate the effects of high‐fat diet on inflammation and metabolism

Disturbances of sleep and circadian rhythms: novel risk factors for obesity

Interplay of central and peripheral circadian clocks in energy metabolism regulation

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