The circadian clock in the suprachiasmatic nucleus of the hypothalamus (SCN) contains multiple autonomous single-cell circadian oscillators and their basic intracellular oscillatory mechanism is beginning to be identified. Less well understood is how individual SCN cells create an integrated tissue pacemaker that produces a coherent read-out to the rest of the organism. Intercellular coupling mechanisms must coordinate individual cellular periods to generate the averaged, genotype-specific circadian period of whole animals. To noninvasively dissociate this circadian oscillatory network in vivo, we (T.C. and A.D.-N.) have developed an experimental paradigm that exposes animals to exotic light-dark (LD) cycles with periods close to the limits of circadian entrainment. If individual oscillators with different periods are loosely coupled within the network, perhaps some of them would be synchronized to the external cycle while others remain unentrained. In fact, rats exposed to an artificially short 22 hr LD cycle express two stable circadian motor activity rhythms with different period lengths in individual animals. Our analysis of SCN gene expression under such conditions suggests that these two motor activity rhythms reflect the separate activities of two oscillators in the anatomically defined ventrolateral and dorsomedial SCN subdivisions. Our "forced desychronization" protocol has allowed the first stable separation of these two regional oscillators in vivo, correlating their activities to distinct behavioral outputs, and providing a powerful approach for understanding SCN tissue organization and signaling mechanisms in behaving animals.
The timing of food intake has been associated with obesity and adverse metabolic outcomes, independently of the amount or content of food intake and activity level. However, the impact of the variability in the timing of food intake between weekends and weekdays on BMI (body mass index) remains unexplored. To address that, we propose to study a marker of the variability of meal timing on weekends versus weekdays (denominated as ‘eating jet lag’) that could be associated with increments in BMI. This cross-sectional study included 1106 subjects (aged 18–25 years). Linear regression models were used to examine the associations of eating jet lag with BMI and circadian related variables (including chronotype, eating duration, sleep duration, and social jet lag). Subsequently, a hierarchical multivariate regression analysis was conducted to determine whether the association of eating jet lag with BMI was independent of potentially confounding variables (e.g., chronotype and social jet lag). Moreover, restricted cubic splines were calculated to study the shape of the association between eating jet lag and BMI. Our results revealed a positive association between eating jet lag and BMI (p = 0.008), which was independent of the chronotype and social jet lag. Further analysis revealed the threshold of eating jet lag was of 3.5 h or more, from which the BMI could significantly increase. These results provided evidence of the suitability of the eating jet lag, as a marker of the variability in meal timing between weekends and weekdays, for the study of the influence of meal timing on obesity. In a long run, the reduction of the variability between meal timing on weekends versus weekdays could be included as part of food timing guidelines for the prevention of obesity among general population.
Proper functioning of the human circadian timing system is crucial to physical and mental health. Much of what we know about this system is based on experimental protocols that induce the desynchronization of behavioral and physiological rhythms within individual subjects, but the neural (or extraneural) substrates for such desynchronization are unknown. We have developed an animal model of human internal desynchrony in which rats are exposed to artificially short (22-h) light-dark cycles. Under these conditions, locomotor activity, sleep-wake, and slow-wave sleep (SWS) exhibit two rhythms within individual animals, one entrained to the 22-h light-dark cycle and the other free-running with a period >24 h ( >24 h). Whereas core body temperature showed two rhythms as well, further analysis indicates this variable oscillates more according to the >24 h rhythm than to the 22-h rhythm, and that this oscillation is due to an activity-independent circadian regulation. Paradoxical sleep (PS), on the other hand, shows only one freerunning rhythm. Our results show that, similarly to humans, (i) circadian rhythms can be internally dissociated in a controlled and predictable manner in the rat and (ii) the circadian rhythms of sleep-wake and SWS can be desynchronized from the rhythms of PS and core body temperature within individual animals. This model now allows for a deeper understanding of the human timekeeping mechanism, for testing potential therapies for circadian dysrhythmias, and for studying the biology of PS and SWS states in a neurologically intact model.
Obesity and unhealthy eating habits have been associated with irregular sleep–wake patterns during the week, also known as social jet lag. The Mediterranean diet is a healthy pattern related with a better health and sleep quality. However, potential associations with social jet lag remain unexplored. The aim of this study was to examine whether higher social jet lag is linked to lower adherence to the Mediterranean diet and whether it is associated with BMI (Body Mass Index). This cross-sectional study included 534 young adults (18–25 years). Anthropometric parameters, adherence to the Mediterranean diet, chronotype and social jet lag were studied. Our results revealed that individuals with greater social jet lag showed lower adherence to the Mediterranean diet and had a higher BMI. Among the habits that characterized the Mediterranean dietary pattern, we observed that higher social jet lag was significantly associated with a lower intake of fruits and vegetables, as well as skipping breakfast. Hence, the promotion of regular sleep habits together with healthy dietary patterns should be considered for obesity prevention, especially among young adults.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.