Endocrine regulation of circadian physiology

Tsang, Anthony H.; Astiz, Mariana; Friedrichs, Maureen; Oster, Henrik

doi:10.1530/joe-16-0051

Cited by 62 publications

(48 citation statements)

References 108 publications

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“…This result is reminiscent of the situation described for the clock control of GC production by the mammalian adrenal gland. In this case circadian cycling in GC titers also depends on a functional central clock (housed in the SCN) as well as a functional peripheral clock in the adrenal gland3, which gate the sensitivity to corticotropin-releasing hormone. The underlying mechanisms are incompletely understood but involve the regulation of cholesterol transport via clock control of Steroidogenic Acute Regulatory protein (StAR) expression.…”

Section: Discussionmentioning

confidence: 99%

“…In animals, many tissues are known to contain circadian pacemakers. Whereas much is currently known about the molecular mechanisms that produce rhythmicity within circadian pacemakers, less is known about how the activity of these pacemakers is coordinated within an animal, even though loss of synchronization between pacemakers can contribute to circadian rhythm and sleep disorders, as well as metabolic and cardiovascular diseases123. In mammals, coordination is effected by the central pacemaker of the suprachiasmatic nucleus (SCN)4 through poorly understood pathways, but which include neural, endocrine56 and even thermal signals7.…”

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confidence: 99%

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Central and peripheral clocks are coupled by a neuropeptide pathway in Drosophila

et al. 2017

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Animal circadian clocks consist of central and peripheral pacemakers, which are coordinated to produce daily rhythms in physiology and behaviour. Despite its importance for optimal performance and health, the mechanism of clock coordination is poorly understood. Here we dissect the pathway through which the circadian clock of Drosophila imposes daily rhythmicity to the pattern of adult emergence. Rhythmicity depends on the coupling between the brain clock and a peripheral clock in the prothoracic gland (PG), which produces the steroid hormone, ecdysone. Time information from the central clock is transmitted via the neuropeptide, sNPF, to non-clock neurons that produce the neuropeptide, PTTH. These secretory neurons then forward time information to the PG clock. We also show that the central clock exerts a dominant role on the peripheral clock. This use of two coupled clocks could serve as a paradigm to understand how daily steroid hormone rhythms are generated in animals.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Central and peripheral clocks are coupled by a neuropeptide pathway in Drosophila

et al. 2017

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“…There is an increasing evidence for the essential roles of the peripheral circadian clocks operative in endocrine tissues for their transcriptional and functional regulation (13–15). Indeed, most of the hormones, including myokines and adipokines, are secreted in a circadian manner and regulated by respective cell-autonomous oscillators (16, 17).…”

Section: Introductionmentioning

confidence: 99%

High-Resolution Recording of the Circadian Oscillator in Primary Mouse α- and β-Cell Culture

2017

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Circadian clocks have been developed in evolution as an anticipatory mechanism allowing for adaptation to the constantly changing light environment due to rotation of the Earth. This mechanism is functional in all light-sensitive organisms. There is a considerable body of evidence on the tight connection between the circadian clock and most aspects of physiology and metabolism. Clocks, operative in the pancreatic islets, have caught particular attention in the last years due to recent reports on their critical roles in regulation of insulin secretion and etiology of type 2 diabetes. While β-cell clocks have been extensively studied during the last years, α-cell clocks and their role in islet function and orchestration of glucose metabolism stayed unexplored, largely due to the difficulty to isolate α-cells, which represents a considerable technical challenge. Here, we provide a detailed description of an experimental approach for the isolation of separate mouse α- and β-cell population, culture of isolated primary α- and β-cells, and their subsequent long-term high-resolution circadian bioluminescence recording. For this purpose, a triple reporter ProGlucagon-Venus/RIP-Cherry/Per2:Luciferase mouse line was established, carrying specific fluorescent reporters for α- and β-cells, and luciferase reporter for monitoring the molecular clockwork. Flow cytometry fluorescence-activated cell sorting allowed separating pure α- and β-cell populations from isolated islets. Experimental conditions, developed by us for the culture of functional primary mouse α- and β-cells for at least 10 days, will be highlighted. Importantly, temporal analysis of freshly isolated α- and β-cells around-the-clock revealed preserved rhythmicity of core clock genes expression. Finally, we describe the setting to assess circadian rhythm in cultured α- and β-cells synchronized in vitro. The here-described methodology allows to analyze the functional properties of primary α- and β-cells under physiological or pathophysiological conditions and to assess the islet cellular clock properties.

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“…3). The disrupted circadian rhythms (Meredith et al 2006) and hyporesponsive HPA axis (Brunton et al 2007) of BK KO mice may be linked through the circadian regulation of the HPA axis and metabolic control, perhaps similar to the circadian and HPA-related control of insulin release (Dickmeis et al 2013;Perelis et al 2015;Tsang et al 2016).…”

Section: Influences Of Construction Vibration/noisementioning

confidence: 99%

Survival and growth of C57BL/6J mice lacking the BK channel,Kcnma1: lower adult body weight occurs together with higher body fat

et al. 2017

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Big conductance potassium (BK) channels contribute to K+ flow and electrical behavior in many cell types. Mice made null for the gene (Kcnma1) producing the BK channel (BKKO) exhibit numerous deficits in physiological functions. Breeding mice lacking a single allele of Kcnma1 (C57BL/6J background) had litter sizes of approximately eight pups. For the period of maternal care (P0–P21), pup deaths peaked at P1 with a second less severe interval of death peaking near P13. Early deaths were twice as likely during a 20‐month period of building construction compared with the quiescent period after cessation of construction. Births during construction were not consistent with Mendelian predictions indicating the likelihood of a specific disadvantage induced by this environmental stressor. Later BKKO pup deaths (~P13) also were more numerous than Mendelian expectations. After weaning, weight gain was slower for BKKO mice compared with wild‐type littermates: 5 g less for male BKKO mice and 4 g less for female BKKO mice. Body composition determined by quantitative magnetic resonance indicated a higher fat proportion for wild‐type female mice compared with males, as well as a higher hydration ratio. Both male and female BKKO mice showed higher fat proportions than wild‐type, with female BKKO mice exhibiting greater variation. Together, these results indicate that BKKO mice suffered disadvantages that lead to prenatal and perinatal death. A metabolic difference likely related to glucose handling led to the smaller body size and distinct composition for BKKO mice, suggesting a diversion of energy supplies from growth to fat storage.

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Endocrine regulation of circadian physiology

Cited by 62 publications

References 108 publications

Central and peripheral clocks are coupled by a neuropeptide pathway in Drosophila

Central and peripheral clocks are coupled by a neuropeptide pathway in Drosophila

High-Resolution Recording of the Circadian Oscillator in Primary Mouse α- and β-Cell Culture

Survival and growth of C57BL/6J mice lacking the BK channel,Kcnma1: lower adult body weight occurs together with higher body fat

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