Frequent Shifts During Chronic Jet Lag Uncouple Liver Rhythms from the Light Cycle in Male Mice
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ABSTRACT:
ORGANISM(S): Mus musculus (mouse)
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PROVIDER: S-BSST1673 | biostudies-other |
REPOSITORIES: biostudies-other
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Project description:BackgroundEvidence suggests that circadian rhythm disorder is associated with a variety of gastrointestinal diseases, and the circadian rhythm plays a key role in maintaining the homeostasis of intestinal flora. The underlying mechanisms are still not completely identified. This study was aimed to explore whether jet lag-caused circadian disruption influences gut microbiome and its metabolites.MethodsMice were synchronized with 12-h light/dark cycles (control group) or subjected to daily 8-h advance of the light/dark cycle for every 3 days (jet-lagged group). Four months later, fecal samples and jejunal contents were collected and analyzed by 16S rRNA gene sequencing. In addition, fecal samples were subjected to metabolome analysis with ultra-performance liquid chromatography coupled to tandem mass spectrometry (UPLC-MS/MS).ResultsThe results of 16s rRNA sequencing showed that chronic jet lag led to decreased microbial abundance, richness, and diversity in both feces and jejunal contents. ANOSIM analysis revealed significant difference between control and jet-lagged groups. As the colonic microbiome, the abundance of Bacteroidetes phylum was significantly decreased and that of Actinobacteria phylum was increased in jet-lagged mice. Jet lag increased the ratio of Firmicutes to Bacteroidetes, an indicator for the imbalance of gut microbiota. Metabolome analysis of fecal samples showed that the levels of tryptophan and its derivatives were decreased in jet-lagged mice. In addition, fecal levels of secondary bile acids changed under jet lag conditions. Correlation analysis identified associations between tryptophan (and its derivatives) levels and colonic microbiota.ConclusionsThis study presents a comprehensive landscape of gut microbiota and its metabolites in mice subjected to chronic jet lag. The results suggest that circadian disruption may lead to changes in fecal and jejunal microbiota and fecal metabolites. Moreover, our results demonstrate a novel interplay between the gut microbiome and metabolome.
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Project description:Shift work is known to be associated with an increased risk of neurological and psychiatric diseases, but how it contributes to the development of these diseases remains unclear. Chronic jet lag (CJL) induced by shifting light-dark cycles repeatedly is a commonly used protocol to mimic the environmental light/dark changes encountered by shift workers. Here we subjected wildtype mice to CJL and performed positron emission tomography imaging of glucose metabolism to monitor brain activities. We also conducted RNA sequencing using prefrontal cortex and nucleus accumbens tissues from these animals, which are brain regions strongly implicated in the pathology of various neurological and psychiatric conditions. Our results reveal the alterations of brain activities and systematic reprogramming of gene expression in brain tissues under CJL, building hypothesis for how CJL increases the susceptibility to neurological and psychiatric diseases.
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Project description:Chronic jet lag (CJL) induced by shifting light-dark cycles repeatedly is a commonly used protocol to mimic the environmental light/dark changes encountered by shift workers. We conducted RNA sequencing using prefrontal cortex (PFC) and nucleus accumbens (NAc) tissues from these animals, which are brains regions strongly implicated in the pathology of various neurological and psychiatric conditions. Our results reveal the alterations of brain activities and systematic reprogramming of gene expression in brain tissues under CJL, building hypothesis for how CJL increases the susceptibility to neurological and psychiatric diseases.
2020-10-01 | GSE153540 | GEO
Project description:Chronic jet lag, a model of shiftwork, increases mortality in aged mice. One potential reason for this association is that the chronic desynchronization between the internal clock phase and the environmental light/dark (LD) cycle might increase the mortality rate. However, this hypothesis has not been examined because of the lack of an appropriate animal model to prove this speculation. Here, we found that rapidly entrainable vasopressin receptor V1a-/-V1b-/- mice showed lower mortality under a chronic jet lag condition. Moreover, we found that pharmacological inactivation of V1a and V1b signaling decreased mortality even in aged wild-type mice, thus providing a potential pharmaceutical intervention for shiftwork-related health problems.
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Project description:Travel across multiple time zones results in desynchronization of environmental time cues and the sleep-wake schedule from their normal phase relationships with the endogenous circadian system. Circadian misalignment can result in poor neurobehavioral performance, decreased sleep efficiency, and inappropriately timed physiological signals including gastrointestinal activity and hormone release. Frequent and repeated transmeridian travel is associated with long-term cognitive deficits, and rodents experimentally exposed to repeated schedule shifts have increased death rates. One approach to reduce the short-term circadian, sleep-wake, and performance problems is to use mathematical models of the circadian pacemaker to design countermeasures that rapidly shift the circadian pacemaker to align with the new schedule. In this paper, the use of mathematical models to design sleep-wake and countermeasure schedules for improved performance is demonstrated. We present an approach to designing interventions that combines an algorithm for optimal placement of countermeasures with a novel mode of schedule representation. With these methods, rapid circadian resynchrony and the resulting improvement in neurobehavioral performance can be quickly achieved even after moderate to large shifts in the sleep-wake schedule. The key schedule design inputs are endogenous circadian period length, desired sleep-wake schedule, length of intervention, background light level, and countermeasure strength. The new schedule representation facilitates schedule design, simulation studies, and experiment design and significantly decreases the amount of time to design an appropriate intervention. The method presented in this paper has direct implications for designing jet lag, shift-work, and non-24-hour schedules, including scheduling for extreme environments, such as in space, undersea, or in polar regions.
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Project description:For many years now a treatment mitigating the debilitating effects of jet lag has been sought. Rapid travel across time zones leads, in most people, to temporary symptoms, in particular poor sleep, daytime alertness and poor performance. Mis-timed circadian rhythms are considered to be the main factor underlying jet-lag symptoms, together with the sleep deprivation from long haul flights. Virtually all aspects of physiology are rhythmic, from cells to systems, and circadian rhythms are coordinated by a central pacemaker or clock in the suprachiasmatic nucleus (SCN) of the hypothalamus. The SCN adapts slowly to changes in time zone, and peripheral clocks or oscillators adapt at different rates, such that the organism is in a state of desynchrony from the external environment and internally. Light exposure is the main factor controlling the circadian system and needs to be considered together with any pharmacological interventions. This review covers the relatively new chronobiotic drugs, which can hasten adaptation of the circadian system, together with drugs directly affecting alertness and sleep propensity. No current treatment can instantly shift circadian phase to a new time zone; however, adaptation can be hastened. The melatoninergic drugs are promising but larger trials in real-life situations are needed. For short stopovers it is recommended to preserve sleep and alertness without necessarily modifying the circadian system. New research suggests that modification of clock function via genetic manipulation may one day have clinical applications.
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Project description:Laboratory studies have demonstrated that circadian clocks align physiology and behavior to 24-h environmental cycles. Examination of athletic performance has been used to discern the functions of these clocks in humans outside of controlled settings. Here, we examined the effects of jet lag, that is, travel that shifts the alignment of 24-h environmental cycles relative to the endogenous circadian clock, on specific performance metrics in Major League Baseball. Accounting for potential differences in home and away performance, travel direction, and team confounding variables, we observed that jet-lag effects were largely evident after eastward travel with very limited effects after westward travel, consistent with the >24-h period length of the human circadian clock. Surprisingly, we found that jet lag impaired major parameters of home-team offensive performance, for example, slugging percentage, but did not similarly affect away-team offensive performance. On the other hand, jet lag impacted both home and away defensive performance. Remarkably, the vast majority of these effects for both home and away teams could be explained by a single measure, home runs allowed. Rather than uniform effects, these results reveal surprisingly specific effects of circadian misalignment on athletic performance under natural conditions.
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Project description:Understanding entrainment of circadian rhythms is a central goal of chronobiology. Many factors, such as period, amplitude, Zeitgeber strength, and daylength, govern entrainment ranges and phases of entrainment. We have tested whether simple amplitude-phase models can provide insight into the control of entrainment phases. Using global optimization, we derived conceptual models with just three free parameters (period, amplitude, and relaxation rate) that reproduce known phenotypic features of vertebrate clocks: phase response curves (PRCs) with relatively small phase shifts, fast re-entrainment after jet lag, and seasonal variability to track light onset or offset. Since optimization found multiple sets of model parameters, we could study this model ensemble to gain insight into the underlying design principles. We found complex associations between model parameters and entrainment features. Arnold onions of representative models visualize strong dependencies of entrainment on periods, relative Zeitgeber strength, and photoperiods. Our results support the use of oscillator theory as a framework for understanding the entrainment of circadian clocks.
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Project description:The advent of artificial lighting, particularly during the evening and night, has significantly altered the predictable daily light and dark cycles in recent times. Altered light environments disrupt the biological clock and negatively impact mood and cognition. Although adolescents commonly experience chronic changes in light/dark cycles, our understanding of how the adolescents' brain adapts to altered light environments remains limited. Here, we investigated the impact of chronic light cycle disruption (LCD) during adolescence, exposing adolescent mice to 19 h of light and 5 h of darkness for 5 days and 12 L:12D for 2 days per week (LCD group) for 4 weeks. We showed that LCD exposure did not affect circadian locomotor activity but impaired memory and increased avoidance response in adolescent mice. Clock gene expression and neuronal activity rhythms analysis revealed that LCD disrupted local molecular clock and neuronal activity in the dentate gyrus (DG) and in the medial amygdala (MeA) but not in the circadian pacemaker (SCN). In addition, we characterized the photoresponsiveness of the MeA and showed that somatostatin neurons are affected by acute and chronic aberrant light exposure during adolescence. Our research provides new evidence highlighting the potential consequences of altered light environments during pubertal development on neuronal physiology and behaviors.
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