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  • 1
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    Disruption of the clock components CLOCK and BMAL1 leads to hypoinsulinaemia and diabetes (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-06-22
    Description: The molecular clock maintains energy constancy by producing circadian oscillations of rate-limiting enzymes involved in tissue metabolism across the day and night. During periods of feeding, pancreatic islets secrete insulin to maintain glucose homeostasis, and although rhythmic control of insulin release is recognized to be dysregulated in humans with diabetes, 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 signalling is delayed in circadian mutant mice, and both Clock and Bmal1 (also called Arntl) mutants show 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. Notably, conditional ablation of the pancreatic clock causes diabetes mellitus due to defective beta-cell function at the very latest stage of stimulus-secretion coupling. These results demonstrate a role for the beta-cell clock in coordinating insulin secretion with the sleep-wake cycle, and reveal that ablation of the pancreatic clock can trigger the onset of diabetes mellitus.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920067/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920067/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marcheva, Biliana -- Ramsey, Kathryn Moynihan -- Buhr, Ethan D -- Kobayashi, Yumiko -- Su, Hong -- Ko, Caroline H -- Ivanova, Ganka -- Omura, Chiaki -- Mo, Shelley -- Vitaterna, Martha H -- Lopez, James P -- Philipson, Louis H -- Bradfield, Christopher A -- Crosby, Seth D -- JeBailey, Lellean -- Wang, Xiaozhong -- Takahashi, Joseph S -- Bass, Joseph -- P01 AG011412/AG/NIA NIH HHS/ -- P01 AG011412-080011/AG/NIA NIH HHS/ -- R01 HL097817/HL/NHLBI NIH HHS/ -- R01 HL097817-01/HL/NHLBI NIH HHS/ -- R37 ES005703/ES/NIEHS NIH HHS/ -- R37-ES-005703/ES/NIEHS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Jul 29;466(7306):627-31. doi: 10.1038/nature09253.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20562852" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/deficiency/*genetics/metabolism ; Aging/genetics/pathology ; Animals ; Blood Glucose/analysis/metabolism ; CLOCK Proteins/deficiency/*genetics/metabolism ; Cell Proliferation ; Cell Size ; Cell Survival ; Circadian Rhythm/genetics/*physiology ; Diabetes Mellitus/genetics/*metabolism ; Gene Expression Profiling ; Glucose Intolerance/genetics ; Glucose Tolerance Test ; In Vitro Techniques ; Insulin/*blood/metabolism/secretion ; Islets of Langerhans/*metabolism/pathology/secretion ; Mice ; Period Circadian Proteins/genetics/metabolism ; Phenotype ; Sleep/genetics/physiology ; Synaptic Vesicles/metabolism ; Wakefulness/genetics/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Circadian clock NAD+ cycle drives mitochondrial oxidative metabolism in mice (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-09-21
    Description: Circadian clocks are self-sustained cellular oscillators that synchronize oxidative and reductive cycles in anticipation of the solar cycle. We found that the clock transcription feedback loop produces cycles of nicotinamide adenine dinucleotide (NAD(+)) biosynthesis, adenosine triphosphate production, and mitochondrial respiration through modulation of mitochondrial protein acetylation to synchronize oxidative metabolic pathways with the 24-hour fasting and feeding cycle. Circadian control of the activity of the NAD(+)-dependent deacetylase sirtuin 3 (SIRT3) generated rhythms in the acetylation and activity of oxidative enzymes and respiration in isolated mitochondria, and NAD(+) supplementation restored protein deacetylation and enhanced oxygen consumption in circadian mutant mice. Thus, circadian control of NAD(+) bioavailability modulates mitochondrial oxidative function and organismal metabolism across the daily cycles of fasting and feeding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3963134/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3963134/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peek, Clara Bien -- Affinati, Alison H -- Ramsey, Kathryn Moynihan -- Kuo, Hsin-Yu -- Yu, Wei -- Sena, Laura A -- Ilkayeva, Olga -- Marcheva, Biliana -- Kobayashi, Yumiko -- Omura, Chiaki -- Levine, Daniel C -- Bacsik, David J -- Gius, David -- Newgard, Christopher B -- Goetzman, Eric -- Chandel, Navdeep S -- Denu, John M -- Mrksich, Milan -- Bass, Joseph -- 5P01HL071643-10/HL/NHLBI NIH HHS/ -- 5P30AR057216-05/AR/NIAMS NIH HHS/ -- F30 DK085936/DK/NIDDK NIH HHS/ -- F30 ES019815/ES/NIEHS NIH HHS/ -- F32 DK092034/DK/NIDDK NIH HHS/ -- P01 AG011412/AG/NIA NIH HHS/ -- P01AG011412-16/AG/NIA NIH HHS/ -- P01DK58398/DK/NIDDK NIH HHS/ -- P30 CA014520/CA/NCI NIH HHS/ -- R01 AG038679/AG/NIA NIH HHS/ -- R01 CA152601-01/CA/NCI NIH HHS/ -- R01 CA152799-01A1/CA/NCI NIH HHS/ -- R01 CA16383801A1/CA/NCI NIH HHS/ -- R01 CA168292/CA/NCI NIH HHS/ -- R01 CA168292-01A1/CA/NCI NIH HHS/ -- R01 DK090242/DK/NIDDK NIH HHS/ -- R01 DK090625/DK/NIDDK NIH HHS/ -- R01 GM065386/GM/NIGMS NIH HHS/ -- R01 HL097817/HL/NHLBI NIH HHS/ -- R01DK090242-03/DK/NIDDK NIH HHS/ -- R01DK090625-01A1/DK/NIDDK NIH HHS/ -- R01HL097817-01/HL/NHLBI NIH HHS/ -- R37 GM059785/GM/NIGMS NIH HHS/ -- T32 DK007169/DK/NIDDK NIH HHS/ -- T32 GM008152/GM/NIGMS NIH HHS/ -- T32 HL007909/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Nov 1;342(6158):1243417. doi: 10.1126/science.1243417. Epub 2013 Sep 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24051248" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/genetics/metabolism ; Acetylation ; Animals ; Circadian Clocks/genetics/*physiology ; *Energy Metabolism ; Fasting ; Lipid Metabolism ; Liver/metabolism ; Mice ; Mice, Knockout ; Mitochondria, Liver/*metabolism ; NAD/*metabolism ; Oxidation-Reduction ; Oxygen Consumption ; Sirtuin 3/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Pancreatic beta cell enhancers regulate rhythmic transcription of genes controlling insulin secretion (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-11-07
    Description: The mammalian transcription factors CLOCK and BMAL1 are essential components of the molecular clock that coordinate behavior and metabolism with the solar cycle. Genetic or environmental perturbation of circadian cycles contributes to metabolic disorders including type 2 diabetes. To study the impact of the cell-autonomous clock on pancreatic beta cell function, we examined pancreatic islets from mice with either intact or disrupted BMAL1 expression both throughout life and limited to adulthood. We found pronounced oscillation of insulin secretion that was synchronized with the expression of genes encoding secretory machinery and signaling factors that regulate insulin release. CLOCK/BMAL1 colocalized with the pancreatic transcription factor PDX1 within active enhancers distinct from those controlling rhythmic metabolic gene networks in liver. We also found that beta cell clock ablation in adult mice caused severe glucose intolerance. Thus, cell type-specific enhancers underlie the circadian control of peripheral metabolism throughout life and may help to explain its dysregulation in diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4669216/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4669216/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perelis, Mark -- Marcheva, Biliana -- Ramsey, Kathryn Moynihan -- Schipma, Matthew J -- Hutchison, Alan L -- Taguchi, Akihiko -- Peek, Clara Bien -- Hong, Heekyung -- Huang, Wenyu -- Omura, Chiaki -- Allred, Amanda L -- Bradfield, Christopher A -- Dinner, Aaron R -- Barish, Grant D -- Bass, Joseph -- ES05703/ES/NIEHS NIH HHS/ -- K01 DK105137/DK/NIDDK NIH HHS/ -- P01 AG011412/AG/NIA NIH HHS/ -- P01AG011412/AG/NIA NIH HHS/ -- P60 DK020595/DK/NIDDK NIH HHS/ -- P60DK020595/DK/NIDDK NIH HHS/ -- R01 DK090625/DK/NIDDK NIH HHS/ -- R01 ES005703/ES/NIEHS NIH HHS/ -- R01DK090625/DK/NIDDK NIH HHS/ -- T32 DK007169/DK/NIDDK NIH HHS/ -- T32 GM007281/GM/NIGMS NIH HHS/ -- T32 HL007909/HL/NHLBI NIH HHS/ -- T32GM07281/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2015 Nov 6;350(6261):aac4250. doi: 10.1126/science.aac4250.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. ; Center for Genetic Medicine, Northwestern University, Chicago, IL 60611, USA. ; Medical Scientist Training Program, University of Chicago, Chicago, IL 60637, USA. Graduate Program in the Biophysical Sciences, University of Chicago, Chicago, IL 60637, USA. James Franck Institute, University of Chicago, Chicago, IL 60637, USA. ; McArdle Laboratory for Cancer Research, University of Wisconsin, Madison, WI 52705, USA. ; Graduate Program in the Biophysical Sciences, University of Chicago, Chicago, IL 60637, USA. James Franck Institute, University of Chicago, Chicago, IL 60637, USA. Department of Chemistry, University of Chicago, Chicago, IL 60637, USA. ; Department of Medicine, Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. j-bass@northwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26542580" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/genetics/metabolism ; Animals ; CLOCK Proteins/metabolism ; Circadian Rhythm/*genetics ; Diabetes Mellitus, Type 2/genetics/metabolism ; Enhancer Elements, Genetic/*physiology ; Exocytosis/genetics ; *Gene Expression Regulation ; Glucose Intolerance ; Homeodomain Proteins/metabolism ; Humans ; Insulin/*secretion ; Insulin-Secreting Cells/*secretion ; Liver/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Trans-Activators/metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Genetic suppression of the circadian Clock mutation by the melatonin biosynthesis pathway (2010)
    National Academy of Sciences
    Details
    Publication Date: 2010-04-19
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 5
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    Rapid precipitation of relativistic electron by EMIC rising‐tone emissions observed by the Van Allen Probes (2019)
    Wiley
    Details
    Publication Date: 2019
    Description: Abstract On 23 February 2014, Van Allen Probes sensors observed quite strong electromagnetic ion cyclotron waves (EMIC) in the outer dayside magnetosphere. The maximum amplitude was more than 14 nT, comparable to 7 % of the magnitude of the ambient magnetic field. The EMIC waves consisted of a series of coherent rising tone emissions. Rising tones are excited sporadically by energetic protons. At the same time, the probes detected drastic fluctuations in fluxes of MeV electrons. It was found that the electron fluxes decreased by more than 30 % during the one minute following the observation of each EMIC rising tone emissions. Furthermore, it is concluded that the flux reduction is a non‐adiabatic (irreversible) process since holes in the particle flux levels appear as drift echoes with energy dispersion. We examine the process of the electron pitch angle scattering by nonlinear wave trapping due to anomalous cyclotron resonance with EMIC rising tone emissions. The energy range of precipitated electrons corresponds to the presumed energy for the threshold amplitude for nonlinear wave trapping. This is the first report of rapid precipitation (〈1 minute) by the mechanism of relativistic electrons by EMIC rising tone emissions and their drift echoes in time observed by spacecraft.
    Print ISSN: 2169-9380
    Electronic ISSN: 2169-9402
    Topics: Geosciences , Physics
    Published by Wiley on behalf of American Geophysical Union (AGU).
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