Chronic circadian desynchronization decreases the  survival of animals with cardiomyopathic heart disease

Penev, Plamen D.; Kolker, Daniel E.; Zee, Phyllis C.; Turek, Fred W.

doi:10.1152/ajpheart.1998.275.6.h2334

Cited by 138 publications

(126 citation statements)

References 19 publications

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“…It has been proposed that GCs are one of the pathways by which the SCN synchronizes the peripheral oscillators (Le Minh et al 2001). This is critically important for organizing the metabolism of the whole body (Penev et al 1998). The findings of the present study may thus be useful for further investigations on this topic.…”

Section: Glucose Tolerance Testmentioning

confidence: 53%

Impaired daily glucocorticoid rhythm in Per1 Brd mice

et al. 2006

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Biological clocks have evolved in all kinds of organisms in order to anticipate and adjust to the daily light-dark cycle. Within the last decade, the molecular machinery underlying the circadian system was unraveled. In the present study, the impact of the loss of the Per1 or Per2 genes, key components of the core clock oscillator, on body mass, food and water intake, glucose metabolism, and hypothalamic-pituitary-adrenal axis, was investigated in the Per1 Brd and Per2 Brd mouse models. The results reveal that the lack of Per1 but not Per2 has severe consequences for the regulation of these parameters. Specifically, in Per1 Brd animals, we found an impaired daily glucocorticoid rhythm, with markedly elevated levels during the day compared to control animals. In addition, Per1 Brd mice showed significant differences in body mass as well as food and water intake. Although the Per1 Brd are lighter than wildtype mice, food and water intake per gram body mass is elevated. In addition, the Per1 Brd mice exhibit an increased glucose metabolism after i.p. injection with glucose. In conclusion, our study presents first evidence for a link between an altered metabolism in Per1 and Per2 deficient mice, which in the case of the Per1 Brd animals might be due to an impaired corticosterone rhythm.

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Section: Glucose Tolerance Testmentioning

confidence: 53%

Impaired daily glucocorticoid rhythm in Per1 Brd mice

et al. 2006

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“…Whether meals scheduled at abnormal circadian times, as occurs during shift work, also leads to such ''internal desynchronization'' in humans has yet to be determined. In some animal models, repeated shifts in the light/dark cycle-typical of shift workleads to premature death, while mutations of circadian clock genes can lead to signs of metabolic syndrome (11,26,27), supporting the potential negative health consequences of circadian disturbances.…”

Section: Discussionmentioning

confidence: 99%

Adverse metabolic and cardiovascular consequences of circadian misalignment

Scheer

Hilton

Mantzoros

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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1,489

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There is considerable epidemiological evidence that shift work is associated with increased risk for obesity, diabetes, and cardiovascular disease, perhaps the result of physiologic maladaptation to chronically sleeping and eating at abnormal circadian times. To begin to understand underlying mechanisms, we determined the effects of such misalignment between behavioral cycles (fasting/ feeding and sleep/wake cycles) and endogenous circadian cycles on metabolic, autonomic, and endocrine predictors of obesity, diabetes, and cardiovascular risk. Ten adults (5 female) underwent a 10-day laboratory protocol, wherein subjects ate and slept at all phases of the circadian cycle-achieved by scheduling a recurring 28-h ''day.'' Subjects ate 4 isocaloric meals each 28-h ''day.'' For 8 days, plasma leptin, insulin, glucose, and cortisol were measured hourly, urinary catecholamines 2 hourly (totaling Ϸ1,000 assays/ subject), and blood pressure, heart rate, cardiac vagal modulation, oxygen consumption, respiratory exchange ratio, and polysomnographic sleep daily. Core body temperature was recorded continuously for 10 days to assess circadian phase. Circadian misalignment, when subjects ate and slept Ϸ12 h out of phase from their habitual times, systematically decreased leptin (؊17%, P < 0.001), increased glucose (؉6%, P < 0.001) despite increased insulin (؉22%, P ‫؍‬ 0.006), completely reversed the daily cortisol rhythm (P < 0.001), increased mean arterial pressure (؉3%, P ‫؍‬ 0.001), and reduced sleep efficiency (؊20%, P < 0.002). Notably, circadian misalignment caused 3 of 8 subjects (with sufficient available data) to exhibit postprandial glucose responses in the range typical of a prediabetic state. These findings demonstrate the adverse cardiometabolic implications of circadian misalignment, as occurs acutely with jet lag and chronically with shift work. autonomic nervous system ͉ diabetes ͉ glucose metabolism ͉ leptin ͉ obesity A pproximately 8.6 million Americans perform shift work (1), which is associated with increased risk of obesity, diabetes, and cardiovascular disease (2-6). The endogenous circadian timing system, including the suprachiasmatic nucleus (SCN) in the hypothalamus and peripheral oscillators in vital organs, optimally regulates much of our physiology and behavior across the 24-h day when it is properly aligned with the sleep/wake cycle. However, shift work is generally associated with chronic misalignment between the endogenous circadian timing system and the behavioral cycles, including sleep/wake and fasting/ feeding cycles (7,8). Shift workers often experience symptoms akin to jet lag, with gastrointestinal complaints, fatigue, and sleepiness during the scheduled wake periods, and poor sleep during the daytime sleep attempts (9). Moreover, chronic circadian misalignment has been proposed to be the underlying cause for the adverse metabolic and cardiovascular health effects of shift work (10, 11). The SCN regulates circadian rhythms in leptin, plasma glucose, glucose tolerance, corticosteroids, and ...

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“…Indeed, shift work has been linked to increased BMI and higher rates of gastrointestinal disorders, cardiovascular disease, as well as diabetes [36]. Few animal models of ''shift work'' have been developed, but one provocative study demonstrated that reversing the light:dark cycle on a weekly basis hastened death in cardiomyopathic hamsters, suggesting that circadian desynchronization may have exacerbated and complicated the pre-disposed disease state in these animals [37].…”

Section: The Circadian Clock: External and Internal Synchronizationmentioning

confidence: 99%

Sleep and circadian rhythms: Key components in the regulation of energy metabolism

et al. 2007

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In this review, we present evidence from human and animal studies to evaluate the hypothesis that sleep and circadian rhythms have direct impacts on energy metabolism, and represent important mechanisms underlying the major health epidemics of obesity and diabetes. The first part of this review will focus on studies that support the idea that sleep loss and obesity are ''interacting epidemics.'' The second part will discuss recent evidence that the circadian clock system plays a fundamental role in energy metabolism at both the behavioral and molecular levels. These lines of research must be seen as in their infancy, but nevertheless, have provided a conceptual and experimental framework that potentially has great importance for understanding metabolic health and disease. OverviewA major aspect of virtually all behavioral and physiological processes is daily variation mediated by the circadian timing system. Diurnal rhythms are generated by an internal biological clock that is synchronized to the 24-h day by environmental cues, primarily the light:dark cycle. When external timing signals are absent, the 24-h rhythms ''free run'' with a period close to 24 h, and are called ''circadian'' (about a day) rhythms. Many rhythms are overt and easy to recognize, such as the sleep-wake cycle, locomotor activity, and feeding behavior. The sleep-wake cycle is arguably the master output rhythm of the circadian clock, because the regulation of most behaviors and physiological activities depend on whether the organism is asleep or awake. A wide-range of less-easily observed rhythms occurs internally and includes the daily regulation of body temperature, adrenal corticosterone and pituitary hormone release, neuropeptide and neurotransmitter levels, sympathetic activation, energy metabolism (e.g., lipolysis, gluconeogenesis, insulin sensitivity, basal metabolic rate), as well as gene transcription. The evolution of a circadian system suggests that the ability of an organism to coordinate itself with the environment (external synchronization) and to maintain temporal organization of endogenous processes (internal synchronization) confers optimal health and survival potential. As we begin to unravel the many links between sleep, circadian rhythms, and metabolism, the survival benefits of temporal organization are beginning to emerge.The first mammalian circadian clock gene was discovered in 1997 by researchers at Northwestern University, and was given the name Clock (Circadian locomotor output cycles kaput), to represent the altered circadian phenotype in the Clock mutant mouse [1,2]. Since that time, there have been major advances in understanding the molecular basis of the circadian clock, including the discovery of many other circadian clock genes and the ongoing elucidation of transcriptional-translational feedback loops through which these clock genes interact [3]. Two important studies in the Clock mutant mouse provided evidence that circadian clock genes may be involved in more than just keeping time. First, it wa...

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Chronic circadian desynchronization decreases the survival of animals with cardiomyopathic heart disease

Cited by 138 publications

References 19 publications

Impaired daily glucocorticoid rhythm in Per1 Brd mice

Impaired daily glucocorticoid rhythm in Per1 Brd mice

Adverse metabolic and cardiovascular consequences of circadian misalignment

Sleep and circadian rhythms: Key components in the regulation of energy metabolism

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