Central Circadian Clock Regulates Energy Metabolism

Ding, Guo‐Lian; Gong, Yingyun; Eckel‐Mahan, Kristin; Sun, Zheng

doi:10.1007/978-981-13-1286-1_5

Cited by 20 publications

(14 citation statements)

References 192 publications

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“…Energy imbalance is associated with the development of obesity and NAFLD. It has been reported that food intake is suppressed in animals exposed to constant light 33 . In ND‐fed rats, the present study also showed a decrease in energy intake subjected to continuous light.…”

Section: Discussionsupporting

confidence: 75%

Effects of constant light exposure on sphingolipidomics and progression of NASH in high‐fat‐fed rats

Yue

Xia

Lin

et al. 2020

J of Gastro and Hepatol

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Background and Aim Non‐alcoholic fatty liver disease (NAFLD) is a growing public health concern worldwide. With the progression of urbanization, light pollution is becoming an inevitable risk factor for NAFLD. However, the role of light pollution on NAFLD is insufficiently understood, and the underlying mechanism remains unclear. The present study explored effects of constant light exposure on NAFLD and elucidated its related mechanisms. Methods Thirty‐two male Sprague Dawley rats were divided into four groups (n = 8 each): (i) rats on a normal diet exposed to standard light–dark cycle (ND‐LD); (ii) rats on a normal diet exposed to constant light (ND‐LL); (iii) rats on a high‐fat diet exposed to standard light–dark cycle (HFD‐LD); and (iv) and rats on a high‐fat diet exposed to constant light (HFD‐LL). After 12 weeks of treatment, rats were sacrificed and pathophysiological assessments were performed. Targeted lipidomics was used to measure sphingolipids, including ceramides, glucosylceramides, and lactosylceramides, sphingomyelins, and sphingosine‐1‐phosphates in plasma and liver tissues. Results In normal chow rats, constant light exposure led to glucose abnormalities and dyslipidemia. In high‐fat‐fed rats, constant light exposure exacerbated glucose abnormalities, dyslipidemia, insulin resistance, and inflammation and aggravated steatohepatitis. Compared with HFD‐LD rats, HFD‐LL had decreased plasma sphingosine‐1‐phosphate and elevated liver concentrations of total ceramide and specific ceramide species (ceramide d18:0/24:0, ceramide d18:1/22:0, ceramide d18:1/24:0, and ceramide d18:1/24:1), which were associated with increased hepatocyte apoptosis. Conclusions Constant light exposure causes dysregulation of sphingolipids and promotes steatohepatitis in high‐fat‐fed rats.

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Section: Discussionsupporting

confidence: 75%

Effects of constant light exposure on sphingolipidomics and progression of NASH in high‐fat‐fed rats

Yue

Xia

Lin

et al. 2020

J of Gastro and Hepatol

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“…In a population of healthcare workers, the phase shift of the master clock after 3-4 consecutive nightshifts could be 71% accounted for by intensity of light exposure according to the individual's baseline phase response curve (81). The SCN clock in turn regulates system wide energy metabolism as well as activity and food seeking behavior in alignment with these light-entrained rhythms (82). This finding helps to explain why, independent of other lifestyle factors (e.g., sleep duration, physical activity, and smoking), light at night (LAN) has been correlated with the increased risk of developing obesity in humans (83) and has been shown to acutely induce glucose intolerance in rats (84).…”

Section: Light At Nightmentioning

confidence: 99%

Feeding Rhythms and the Circadian Regulation of Metabolism

2020

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The molecular circadian clock regulates metabolic processes within the cell, and the alignment of these clocks between tissues is essential for the maintenance of metabolic homeostasis. The possibility of misalignment arises from the differential responsiveness of tissues to the environmental cues that synchronize the clock (zeitgebers). Although light is the dominant environmental cue for the master clock of the suprachiasmatic nucleus, many other tissues are sensitive to feeding and fasting. When rhythms of feeding behavior are altered, for example by shift work or the constant availability of highly palatable foods, strong feedback is sent to the peripheral molecular clocks. Varying degrees of phase shift can cause the systemic misalignment of metabolic processes. Moreover, when there is a misalignment between the endogenous rhythms in physiology and environmental inputs, such as feeding during the inactive phase, the body's ability to maintain homeostasis is impaired. The loss of phase coordination between the organism and environment, as well as internal misalignment between tissues, can produce cardiometabolic disease as a consequence. The aim of this review is to synthesize the work on the mechanisms and metabolic effects of circadian misalignment. The timing of food intake is highlighted as a powerful environmental cue with the potential to destroy or restore the synchrony of circadian rhythms in metabolism.

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“…90 Eating late can cause circadian disruption, resulting in production of free cortisol, changes in daily rhythms of body temperature, decreased resting energy expenditure, and decreased glucose tolerance. 91,92 Thus, timing of meals could have serious implications not only for weight management, but also for development of cardiovascular disease. A recent review confirmed that skipping breakfast increased the risk of overweight and obesity.…”

Section: Meal Timingmentioning

confidence: 99%