Circadian rhythm of adrenal glucocorticoid: its regulation and clinical implications.
TL;DR: Recent chronobiological research strongly supports the idea that multiple regulatory mechanisms along with the classical HPA neuroendocrine axis underlie the diurnal rhythm of circulating GC.
About: This article is published in Biochimica et Biophysica Acta.The article was published on 2011-05-01 and is currently open access. It has received 274 citations till now. The article focuses on the topics: Circadian rhythm & Glucocorticoid.
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TL;DR: It is an aim of this review to stimulate research on melatonin signaling in peripheral tissues and discriminate between direct effects of the pineal indoleamine at the target organ and others mediated by modulation of oscillators.
Abstract: Evidence is accumulating regarding the importance of circadian core oscillators, several associated factors, and melatonin signaling in the maintenance of health. Dysfunction of endogenous clocks, melatonin receptor polymorphisms, age- and disease-associated declines of melatonin likely contribute to numerous diseases including cancer, metabolic syndrome, diabetes type 2, hypertension, and several mood and cognitive disorders. Consequences of gene silencing, overexpression, gene polymorphisms, and deviant expression levels in diseases are summarized. The circadian system is a complex network of central and peripheral oscillators, some of them being relatively independent of the pacemaker, the suprachiasmatic nucleus. Actions of melatonin on peripheral oscillators are poorly understood. Various lines of evidence indicate that these clocks are also influenced or phase-reset by melatonin. This includes phase differences of core oscillator gene expression under impaired melatonin signaling, effects of melatonin and melatonin receptor knockouts on oscillator mRNAs or proteins. Cross-connections between melatonin signaling pathways and oscillator proteins, including associated factors, are discussed in this review. The high complexity of the multioscillator system comprises alternate or parallel oscillators based on orthologs and paralogs of the core components and a high number of associated factors with varying tissue-specific importance, which offers numerous possibilities for interactions with melatonin. It is an aim of this review to stimulate research on melatonin signaling in peripheral tissues. This should not be restricted to primary signal molecules but rather include various secondarily connected pathways and discriminate between direct effects of the pineal indoleamine at the target organ and others mediated by modulation of oscillators.
373 citations
TL;DR: Multiple systemic and molecular mechanisms exist that connect the circadian clock with metabolism at all levels, from cellular organelles to the whole organism, and deregulation of this circadian–metabolic crosstalk can lead to various pathologies.
Abstract: Humans, like all mammals, partition their daily behaviour into activity (wakefulness) and rest (sleep) phases that differ largely in their metabolic requirements. The circadian clock evolved as an autonomous timekeeping system that aligns behavioural patterns with the solar day and supports the body functions by anticipating and coordinating the required metabolic programmes. The key component of this synchronization is a master clock in the brain, which responds to light–darkness cues from the environment. However, to achieve circadian control of the entire organism, each cell of the body is equipped with its own circadian oscillator that is controlled by the master clock and confers rhythmicity to individual cells and organs through the control of rate-limiting steps of metabolic programmes. Importantly, metabolic regulation is not a mere output function of the circadian system, but nutrient, energy and redox levels signal back to cellular clocks in order to reinforce circadian rhythmicity and to adapt physiology to temporal tissue-specific needs. Thus, multiple systemic and molecular mechanisms exist that connect the circadian clock with metabolism at all levels, from cellular organelles to the whole organism, and deregulation of this circadian–metabolic crosstalk can lead to various pathologies. Circadian rhythms align organismal functions with phases of rest and activity. Accordingly, circadian oscillations occur in many physiological processes, including various metabolic functions. In turn, metabolic cues are emerging as regulators of the circadian clock. This crosstalk between metabolism and circadian rhythms has important implications for human health.
336 citations
TL;DR: The adrenal gland is still of prime importance for understanding how the oscillations of clock genes in peripheral tissues result in functional rhythms of these tissues, whereas it has become even more evident that adrenal glucocorticoids are key in the resetting of the circadian system after a phase-shift.
333 citations
TL;DR: The present review highlights the inter-relationship between circadian clocks and sex differences and points to ways in which disruption of circadian rhythms within these systems differs in the sexes and is associated with dysfunction and disease.
245 citations
TL;DR: It is argued that the history and foundations of the transrepression hypothesis are critically re-examine, that it is incompatible with the complexity of gene regulation by glucocorticoids and poorly supported by experimental evidence; that it no longer aids clear thinking about the actions of the glucOCorticoid receptor; and that it will not prove a fruitful basis for continued refinement and improvement of anti-inflammatory drugs that target the glucocortex receptor.
193 citations
Cites background from "Circadian rhythm of adrenal glucoco..."
...Under normal conditions, endogenous GC levels in serum display circadian variations that are regulated by the central clock-keeper of the supra-chiasmatic nucleus in the hypothalamus, peaking at the beginning of the period of greatest activity (morning in humans, nightfall in mice and many other rodents) (Nader et al., 2010; Chung et al., 2011; Dickmeis & Foulkes, 2011)....
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...…that are regulated by the central clock-keeper of the supra-chiasmatic nucleus in the hypothalamus, peaking at the beginning of the period of greatest activity (morning in humans, nightfall in mice and many other rodents) (Nader et al., 2010; Chung et al., 2011; Dickmeis & Foulkes, 2011)....
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References
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TL;DR: This review considers recent findings regarding GC action and generates criteria for determining whether a particular GC action permits, stimulates, or suppresses an ongoing stress-response or, as an additional category, is preparative for a subsequent stressor.
Abstract: The secretion of glucocorticoids (GCs) is a classic endocrine response to stress. Despite that, it remains controversial as to what purpose GCs serve at such times. One view, stretching back to the time of Hans Selye, posits that GCs help mediate the ongoing or pending stress response, either via basal levels of GCs permitting other facets of the stress response to emerge efficaciously, and/or by stress levels of GCs actively stimulating the stress response. In contrast, a revisionist viewpoint posits that GCs suppress the stress response, preventing it from being pathologically overactivated. In this review, we consider recent findings regarding GC action and, based on them, generate criteria for determining whether a particular GC action permits, stimulates, or suppresses an ongoing stressresponse or, as an additional category, is preparative for a subsequent stressor. We apply these GC actions to the realms of cardiovascular function, fluid volume and hemorrhage, immunity and inflammation, metabolism, neurobiology, and reproductive physiology. We find that GC actions fall into markedly different categories, depending on the physiological endpoint in question, with evidence for mediating effects in some cases, and suppressive or preparative in others. We then attempt to assimilate these heterogeneous GC actions into a physiological whole. (Endocrine Reviews 21: 55‐ 89, 2000)
6,707 citations
TL;DR: It used to be that research in chronobiology moved biochemical functions [transcriptional activators], the along at a gentlemanly pace, but by mid 1997 the word in determining what the authors perceive as time was PASWCCLK.
2,723 citations
"Circadian rhythm of adrenal glucoco..." refers background in this paper
...It arises from an innate and genetically operated timekeeping system referred to as a “biological clock” [1,2]....
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TL;DR: The transcription factor CREB functions in glucose homeostasis, growth-factor-dependent cell survival, and has been implicated in learning and memory, and how is specificity achieved in these signalling pathways?
Abstract: The transcription factor CREB -- for 'cyclic AMP response element-binding protein' -- functions in glucose homeostasis, growth-factor-dependent cell survival, and has been implicated in learning and memory. CREB is phosphorylated in response to various signals, but how is specificity achieved in these signalling pathways?
2,444 citations
"Circadian rhythm of adrenal glucoco..." refers background in this paper
...transcription factors modulate the expression of genes involved in adrenal GC biosynthesis by binding to the CRE residing in the promoter regions of those genes [52,53]....
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TL;DR: Genetic and genomic analysis suggests that a relatively small number of output genes are directly regulated by core oscillator components, and major processes regulated by the SCN and liver were found to be under circadian regulation.
2,227 citations
TL;DR: It is shown that temporal feeding restriction under light-dark or dark-dark conditions can change the phase of circadian gene expression in peripheral cell types by up to 12 h while leaving thephase of cyclic gene expressionIn the SCN unaffected.
Abstract: In mammals, circadian oscillators exist not only in the suprachiasmatic nucleus, which harbors the central pacemaker, but also in most peripheral tissues. It is believed that the SCN clock entrains the phase of peripheral clocks via chemical cues, such as rhythmically secreted hormones. Here we show that temporal feeding restriction under light–dark or dark–dark conditions can change the phase of circadian gene expression in peripheral cell types by up to 12 h while leaving the phase of cyclic gene expression in the SCN unaffected. Hence, changes in metabolism can lead to an uncoupling of peripheral oscillators from the central pacemaker. Sudden large changes in feeding time, similar to abrupt changes in the photoperiod, reset the phase of rhythmic gene expression gradually and are thus likely to act through a clock-dependent mechanism. Food-induced phase resetting proceeds faster in liver than in kidney, heart, or pancreas, but after 1 wk of daytime feeding, the phases of circadian gene expression are similar in all examined peripheral tissues.
2,083 citations
"Circadian rhythm of adrenal glucoco..." refers background in this paper
...Interestingly, restricted daytime feeding of nocturnal animals can dissociate the phases of the SCN central pacemaker and other peripheral clocks, presumably by food-entrainable oscillators [75]; under this daytime feeding regime, the daily GC profiles are split into 2 peaks each day [76,77], implying the presence of adrenalintrinsic mechanisms....
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