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      Circadian clock control of endocrine factors.

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          Abstract

          Organisms experience dramatic fluctuations in demands and stresses over the course of the day. In order to maintain biological processes within physiological boundaries, mechanisms have evolved for anticipation of, and adaptation to, these daily fluctuations. Endocrine factors have an integral role in homeostasis. Not only do circulating levels of various endocrine factors oscillate over the 24 h period, but so too does responsiveness of target tissues to these signals or stimuli. Emerging evidence suggests that these daily endocrine oscillations do not occur solely in response to behavioural fluctuations associated with sleep-wake and feeding-fasting cycles, but are orchestrated by an intrinsic timekeeping mechanism known as the circadian clock. Disruption of circadian clocks by genetic and/or environmental factors seems to precipitate numerous common disorders, including the metabolic syndrome and cancer. Collectively, these observations suggest that strategies designed to realign normal circadian rhythmicities hold potential for the treatment of various endocrine-related disorders.

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          The orphan nuclear receptor REV-ERBalpha controls circadian transcription within the positive limb of the mammalian circadian oscillator.

          Nicolas Preitner, Francesca Damiola, Luis-Lopez-Molina … (2002)
          Mammalian circadian rhythms are generated by a feedback loop in which BMAL1 and CLOCK, players of the positive limb, activate transcription of the cryptochrome and period genes, components of the negative limb. Bmal1 and Per transcription cycles display nearly opposite phases and are thus governed by different mechanisms. Here, we identify the orphan nuclear receptor REV-ERBalpha as the major regulator of cyclic Bmal1 transcription. Circadian Rev-erbalpha expression is controlled by components of the general feedback loop. Thus, REV-ERBalpha constitutes a molecular link through which components of the negative limb drive antiphasic expression of components of the positive limb. While REV-ERBalpha influences the period length and affects the phase-shifting properties of the clock, it is not required for circadian rhythm generation.
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            Disruption of the Clock Components CLOCK and BMAL1 Leads to Hypoinsulinemia and Diabetes

            Biliana Marcheva, Kathryn Moynihan Ramsey, Ethan D Buhr … (2010)
            The molecular clock maintains energy constancy by producing circadian oscillations of rate-limiting enzymes involved in tissue metabolism across the day and night1–3. During periods of feeding, pancreatic islets secrete insulin to maintain glucose homeostasis, and while rhythmic control of insulin release is recognized to be dysregulated in humans with diabetes4, it is not known how the circadian clock may affect this process. Here we show that pancreatic islets possess self-sustained circadian gene and protein oscillations of the transcription factors CLOCK and BMAL1. The phase of oscillation of islet genes involved in growth, glucose metabolism, and insulin signaling is delayed in circadian mutant mice, and both Clock 5,6 and Bmal1 7 mutants exhibit impaired glucose tolerance, reduced insulin secretion, and defects in size and proliferation of pancreatic islets that worsen with age. Clock disruption leads to transcriptome-wide alterations in the expression of islet genes involved in growth, survival, and synaptic vesicle assembly. Remarkably, conditional ablation of the pancreatic clock causes diabetes mellitus due to defective β-cell function at the very latest stage of stimulus-secretion coupling. These results demonstrate a role for the β-cell clock in coordinating insulin secretion with the sleep-wake cycle, and reveal that ablation of the pancreatic clock can trigger onset of diabetes mellitus.
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              The genetics of mammalian circadian order and disorder: implications for physiology and disease.

              Joseph S Takahashi, Hee-Kyung Hong, Caroline Ko … (2008)
              Circadian cycles affect a variety of physiological processes, and disruptions of normal circadian biology therefore have the potential to influence a range of disease-related pathways. The genetic basis of circadian rhythms is well studied in model organisms and, more recently, studies of the genetic basis of circadian disorders has confirmed the conservation of key players in circadian biology from invertebrates to humans. In addition, important advances have been made in understanding how these molecules influence physiological functions in tissues throughout the body. Together, these studies set the scene for applying our knowledge of circadian biology to the understanding and treatment of a range of human diseases, including cancer and metabolic and behavioural disorders.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Nat Rev Endocrinol
                Title: Nature reviews. Endocrinology
                ISSN (Electronic): 1759-5037
                ISSN (Print): 1759-5029
                Publication date (Electronic): Aug 2014
                Volume: 10
                Issue: 8
                Affiliations
                [1 ] Division of Behavioural Neurobiology, Department of Psychiatry, Department of Medicine, University of Alabama at Birmingham, 703 19th Street South, Birmingham, AL 35294, USA.
                [2 ] Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Alabama at Birmingham, 703 19th Street South, Birmingham, AL 35294, USA.
                [3 ] Division of Cardiovascular Diseases, Department of Medicine, University of Alabama at Birmingham, 703 19th Street South, Birmingham, AL 35294, USA.
                Article
                Publisher Item ID: nrendo.2014.78 Mid ID: NIHMS654698
                DOI: 10.1038/nrendo.2014.78
                PubMed ID: 24863387
                SO-VID: 93218b19-bb58-46af-9deb-901382b460f1
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