Resetting Mechanism of Central and Peripheral Circadian Clocks in Mammals

Hirota, Tsuyoshi; Fukada, Yoshitaka

doi:10.2108/zsj.21.359

Cited by 229 publications

(195 citation statements)

References 131 publications

(128 reference statements)

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“…Phospho-CREB homodimers bind to the promoters of the clock genes Per1 and Per2 thereby activating their expression. As a consequence behavioral activity rhythms in mice and humans are phase advanced or delayed, depending on the time of nocturnal light exposure (reviewed in [79]). …”

Section: The Impact Of Clock Genes On Physiologymentioning

confidence: 99%

The daily rhythm of mice

2011

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Edited by Martha Merrow and Michael BrunnerKeywords: Clock mutant mice Metabolism Cancer Neurological disease Mood Obesity a b s t r a c tThe house mouse Mus musculus represents a valuable tool for the analysis and the understanding of the mammalian circadian oscillator. Forward and reverse genetics allowed the identification of clock components and the verification of their function within the circadian clockwork. In many cases unforeseen links were discovered between a particular circadian regulatory protein and various diseases or syndromes. Thus, this model system is not only perfectly suited to pinpoint the components of the mammalian circadian clock, but also to unravel metabolic, physiological, and pathological processes linked to the circadian timing system.

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Section: The Impact Of Clock Genes On Physiologymentioning

confidence: 99%

The daily rhythm of mice

2011

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“…Circadian regulation is mediated by transcriptional and post-translational modification of a discrete group of genes/proteins (Hirota and Fukada 2004;Lowrey and Takahashi 2004). Transcriptional regulatory proteins belonging to the basic helix-loop-helix/Per-ARNT-single-minded domain family interact with each other and downstream target proteins to create a self-perpetuating, rhythmic pattern of gene transcription.…”

Section: Introductionmentioning

confidence: 99%

“…Outside of the central nervous system, adipose tissue physiology exhibits some of the most robust associations with seasonal, diurnal, and circadian rhythms. The serum levels of glucocorticoids and melatonin, factors with potent adipogenic properties, exhibit circadian oscillations (Hirota and Fukada 2004;Lowrey and Takahashi 2004). Eating during periods of darkness (Holmback et al 2002(Holmback et al , 2003Spiegel et al 2004) and antipsychotic drugs influencing circadian rhythms such as lithium chloride and valproic acid (Baptista et al 1995;Elmslie et al 2001;Atmaca et al 2002;Chengappa et al 2002;Fagiolini et al 2002Fagiolini et al , 2003Iwahana et al 2004) have been associated with an increased incidence of obesity.…”

Section: Introductionmentioning

confidence: 99%

Biological aging alters circadian mechanisms in murine adipose tissue depots

Sutton

Ptitsyn

Floyd

et al. 2012

AGE

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Biological aging alters the metabolism and volume of adipose tissue depots. Recent evidence suggests that circadian mechanisms play a role in promoting adipogenesis, obesity, and lipodystrophy.The current study compared cohorts of younger (5-9 months) and older (24-28 months) C57BL/6 mice as a function of biological age and circadian time. Advanced age significantly reduced the weight of the AGE (2013) 35:533-547 DOI 10.1007 Electronic supplementary material The online version of this article (doi:10.1007/s11357-012-9389-7) contains supplementary material, which is available to authorized users. brown, epididymal, inguinal, and retroperitoneal adipose depots but not total body weight. The older mice reduced their physical activity by >50% and delayed their activity initiation after light offset. The expressed transcriptome in brown and white adipose depots and liver of both cohorts displayed evidence of circadian rhythmicity; however, the oscillating mRNAs differed significantly between age groups and across tissues. The amplitude of Cry1, a component of the negative arm of the circadian apparatus, and downstream regulators such as Rev-erbα were elevated in the older relative to the younger cohorts as a function of circadian time. Overall, transcript levels differed significantly for 557 (inguinal adipose), 1,016 (liver), and 1,021 (brown adipose) expressed sequences between the cohorts as a function of age. These included transcripts encoding proteins within the canonical and non-canonical Wnt pathways. Since the Wnt pathway regulates adipose stem cell differentiation and shares a critical enzyme, glycogen synthase kinase 3β, with the circadian mechanism, the intersection between these two fundamental regulatory mechanisms merits further investigation with respect to biological aging of adipose tissues.

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“…This master clock, which in mammals, resides in the hypothalamic suprachiasmatic nucleus, synchronizes multiple peripheral oscillators to ensure temporally coordinated physiology (6)(7)(8). Clocks outside the brain have been demonstrated by the measurement of free-running rhythms of gene expression in cultured peripheral tissues (9,10).…”

mentioning

confidence: 99%