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  • 1
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    Nuclear receptor corepressor and histone deacetylase 3 govern circadian metabolic physiology (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-11-28
    Description: Rhythmic changes in histone acetylation at circadian clock genes suggest that temporal modulation of gene expression is regulated by chromatin modifications. Furthermore, recent studies demonstrate a critical relationship between circadian and metabolic physiology. The nuclear receptor corepressor 1 (Ncor1) functions as an activating subunit for the chromatin modifying enzyme histone deacetylase 3 (Hdac3). Lack of Ncor1 is incompatible with life, and hence it is unknown whether Ncor1, and particularly its regulation of Hdac3, is critical for adult mammalian physiology. Here we show that specific, genetic disruption of the Ncor1-Hdac3 interaction in mice causes aberrant regulation of clock genes and results in abnormal circadian behaviour. These mice are also leaner and more insulin-sensitive owing to increased energy expenditure. Unexpectedly, loss of a functional Ncor1-Hdac3 complex in vivo does not lead to sustained increases in known catabolic genes, but instead significantly alters the oscillatory patterns of several metabolic genes, demonstrating that circadian regulation of metabolism is critical for normal energy balance. These findings indicate that activation of Hdac3 by Ncor1 is a nodal point in the epigenetic regulation of circadian and metabolic physiology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2742159/" 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/PMC2742159/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alenghat, Theresa -- Meyers, Katherine -- Mullican, Shannon E -- Leitner, Kirstin -- Adeniji-Adele, Adetoun -- Avila, Jacqueline -- Bucan, Maja -- Ahima, Rexford S -- Kaestner, Klaus H -- Lazar, Mitchell A -- DK19525/DK/NIDDK NIH HHS/ -- DK43806/DK/NIDDK NIH HHS/ -- DK49210/DK/NIDDK NIH HHS/ -- DK50306/DK/NIDDK NIH HHS/ -- R37 DK043806/DK/NIDDK NIH HHS/ -- R37 DK043806-15/DK/NIDDK NIH HHS/ -- R37 DK043806-16/DK/NIDDK NIH HHS/ -- R37 DK043806-17/DK/NIDDK NIH HHS/ -- England -- Nature. 2008 Dec 18;456(7224):997-1000. doi: 10.1038/nature07541. Epub 2008 Nov 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19037247" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Amino Acid Substitution ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Biological Clocks/genetics/physiology ; Cells, Cultured ; Circadian Rhythm/genetics/*physiology ; Diet ; Energy Metabolism/genetics/physiology ; Female ; Gene Expression Regulation ; Histone Deacetylases/genetics/*metabolism ; Liver/enzymology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Proteins/chemistry/genetics/*metabolism ; Nuclear Receptor Co-Repressor 1 ; Obesity/enzymology/genetics/metabolism ; Repressor Proteins/chemistry/genetics/*metabolism
    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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    Histone deacetylase 3 coordinates commensal-bacteria-dependent intestinal homeostasis (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-11-05
    Description: The development and severity of inflammatory bowel diseases and other chronic inflammatory conditions can be influenced by host genetic and environmental factors, including signals derived from commensal bacteria. However, the mechanisms that integrate these diverse cues remain undefined. Here we demonstrate that mice with an intestinal epithelial cell (IEC)-specific deletion of the epigenome-modifying enzyme histone deacetylase 3 (HDAC3(DeltaIEC) mice) exhibited extensive dysregulation of IEC-intrinsic gene expression, including decreased basal expression of genes associated with antimicrobial defence. Critically, conventionally housed HDAC3(DeltaIEC) mice demonstrated loss of Paneth cells, impaired IEC function and alterations in the composition of intestinal commensal bacteria. In addition, HDAC3(DeltaIEC) mice showed significantly increased susceptibility to intestinal damage and inflammation, indicating that epithelial expression of HDAC3 has a central role in maintaining intestinal homeostasis. Re-derivation of HDAC3(DeltaIEC) mice into germ-free conditions revealed that dysregulated IEC gene expression, Paneth cell homeostasis and intestinal barrier function were largely restored in the absence of commensal bacteria. Although the specific mechanisms through which IEC-intrinsic HDAC3 expression regulates these complex phenotypes remain to be determined, these data indicate that HDAC3 is a critical factor that integrates commensal-bacteria-derived signals to calibrate epithelial cell responses required to establish normal host-commensal relationships and maintain intestinal homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3949438/" 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/PMC3949438/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alenghat, Theresa -- Osborne, Lisa C -- Saenz, Steven A -- Kobuley, Dmytro -- Ziegler, Carly G K -- Mullican, Shannon E -- Choi, Inchan -- Grunberg, Stephanie -- Sinha, Rohini -- Wynosky-Dolfi, Meghan -- Snyder, Annelise -- Giacomin, Paul R -- Joyce, Karen L -- Hoang, Tram B -- Bewtra, Meenakshi -- Brodsky, Igor E -- Sonnenberg, Gregory F -- Bushman, Frederic D -- Won, Kyoung-Jae -- Lazar, Mitchell A -- Artis, David -- 2-P30 CA016520/CA/NCI NIH HHS/ -- AI061570/AI/NIAID NIH HHS/ -- AI074878/AI/NIAID NIH HHS/ -- AI087990/AI/NIAID NIH HHS/ -- AI095466/AI/NIAID NIH HHS/ -- AI095608/AI/NIAID NIH HHS/ -- AI097333/AI/NIAID NIH HHS/ -- AI102942/AI/NIAID NIH HHS/ -- AI106697/AI/NIAID NIH HHS/ -- DK043806/DK/NIDDK NIH HHS/ -- DP5 OD012116/OD/NIH HHS/ -- DP5OD012116/OD/NIH HHS/ -- F31-GM082187/GM/NIGMS NIH HHS/ -- K08 DK084347/DK/NIDDK NIH HHS/ -- K08 DK093784/DK/NIDDK NIH HHS/ -- K08-DK084347/DK/NIDDK NIH HHS/ -- K08-DK093784/DK/NIDDK NIH HHS/ -- P01 AI106697/AI/NIAID NIH HHS/ -- P30 CA016520/CA/NCI NIH HHS/ -- P30 DK019525/DK/NIDDK NIH HHS/ -- P30-DK050306/DK/NIDDK NIH HHS/ -- P30-DK19525/DK/NIDDK NIH HHS/ -- R01 AI061570/AI/NIAID NIH HHS/ -- R01 AI074878/AI/NIAID NIH HHS/ -- R01 AI095466/AI/NIAID NIH HHS/ -- R01 AI097333/AI/NIAID NIH HHS/ -- R01 AI102942/AI/NIAID NIH HHS/ -- R21 AI083480/AI/NIAID NIH HHS/ -- R21 AI087990/AI/NIAID NIH HHS/ -- R21 AI105346/AI/NIAID NIH HHS/ -- R21-AI105346/AI/NIAID NIH HHS/ -- R37 DK043806/DK/NIDDK NIH HHS/ -- T32-RR007063/RR/NCRR NIH HHS/ -- U01 AI095608/AI/NIAID NIH HHS/ -- England -- Nature. 2013 Dec 5;504(7478):153-7. doi: 10.1038/nature12687. Epub 2013 Nov 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA [2] Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA [3] Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24185009" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Bacteria/genetics ; Colitis, Ulcerative/enzymology/genetics/microbiology ; Crohn Disease/enzymology/genetics/microbiology ; Female ; Gene Deletion ; Gene Expression Profiling ; *Gene Expression Regulation ; Histone Deacetylases/genetics/*metabolism ; *Homeostasis ; Humans ; Intestinal Mucosa/*enzymology/pathology ; Intestines/*microbiology ; Male ; Mice ; Mice, Inbred C57BL ; Paneth Cells/cytology/metabolism ; RNA, Ribosomal, 16S/genetics ; Signal Transduction ; *Symbiosis
    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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  • 3
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    Physiology. The health risk of obesity--better metrics imperative (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ahima, Rexford S -- Lazar, Mitchell A -- P01-DK-049210/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2013 Aug 23;341(6148):856-8. doi: 10.1126/science.1241244.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, and the Institute for Diabetes, Obesity and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA. ahima@mail.med.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23970691" target="_blank"〉PubMed〈/a〉
    Keywords: *Body Mass Index ; Body Weight/*physiology ; Cardiovascular Diseases/epidemiology/mortality ; *Cause of Death ; Diabetes Mellitus/epidemiology/mortality ; Female ; Humans ; Male ; Obesity/*mortality/*physiopathology ; Risk
    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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