دورية أكاديمية
A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism.
| العنوان: | A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism. |
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| المؤلفون: | Pradas-Juni M; Functional Genomics and Metabolism Unit, Department for Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, 5230, Odense M, Denmark.; Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931, Cologne, Germany.; Cologne Cluster of Excellence-Cellular Stress Responses in Ageing-associated Diseases (CECAD), Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931, Cologne, Germany., Hansmeier NR; Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931, Cologne, Germany.; Cologne Cluster of Excellence-Cellular Stress Responses in Ageing-associated Diseases (CECAD), Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931, Cologne, Germany., Link JC; Department of Biological Chemistry, University of California, Los Angeles (UCLA), 650 Charles E. Young Drive South, Los Angeles, CA, 90095, USA.; Department of Medicine, Division of Cardiology, UCLA, 650 Charles E. Young Drive South, Los Angeles, CA, 90095, USA., Schmidt E; Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931, Cologne, Germany.; Cologne Cluster of Excellence-Cellular Stress Responses in Ageing-associated Diseases (CECAD), Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931, Cologne, Germany., Larsen BD; Functional Genomics and Metabolism Unit, Department for Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, 5230, Odense M, Denmark., Klemm P; Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931, Cologne, Germany.; Cologne Cluster of Excellence-Cellular Stress Responses in Ageing-associated Diseases (CECAD), Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931, Cologne, Germany., Meola N; Functional Genomics and Metabolism Unit, Department for Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, 5230, Odense M, Denmark., Topel H; Functional Genomics and Metabolism Unit, Department for Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, 5230, Odense M, Denmark.; Izmir Biomedicine and Genome Center (IBG), Mithatpasa Ave. 58/5, 35340, Izmir, Turkey.; Department of Medical Biology and Genetics, Graduate School of Health Sciences, Dokuz Eylul University, Mithatpasa Ave. 1606, 35330, Izmir, Turkey., Loureiro R; Functional Genomics and Metabolism Unit, Department for Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, 5230, Odense M, Denmark.; Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931, Cologne, Germany.; Cologne Cluster of Excellence-Cellular Stress Responses in Ageing-associated Diseases (CECAD), Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931, Cologne, Germany., Dhaouadi I; Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931, Cologne, Germany.; Cologne Cluster of Excellence-Cellular Stress Responses in Ageing-associated Diseases (CECAD), Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931, Cologne, Germany., Kiefer CA; Functional Genomics and Metabolism Unit, Department for Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, 5230, Odense M, Denmark., Schwarzer R; Cologne Cluster of Excellence-Cellular Stress Responses in Ageing-associated Diseases (CECAD), Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931, Cologne, Germany., Khani S; Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931, Cologne, Germany.; Cologne Cluster of Excellence-Cellular Stress Responses in Ageing-associated Diseases (CECAD), Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931, Cologne, Germany., Oliverio M; Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931, Cologne, Germany.; Cologne Cluster of Excellence-Cellular Stress Responses in Ageing-associated Diseases (CECAD), Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931, Cologne, Germany., Awazawa M; Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931, Cologne, Germany.; Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, 162-8655, Japan., Frommolt P; Cologne Cluster of Excellence-Cellular Stress Responses in Ageing-associated Diseases (CECAD), Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931, Cologne, Germany., Heeren J; Department of Biochemistry and Molecular Cell Biology, Martinistraße 52, 20246, Hamburg, Germany., Scheja L; Department of Biochemistry and Molecular Cell Biology, Martinistraße 52, 20246, Hamburg, Germany., Heine M; Department of Biochemistry and Molecular Cell Biology, Martinistraße 52, 20246, Hamburg, Germany., Dieterich C; Section of Bioinformatics and Systems Cardiology, Klaus Tschira Institute for Integrative Computational Cardiology, University Hospital Heidelberg, Im Neuenheimer Feld 669, 69120, Heidelberg, Germany., Büning H; Institute of Experimental Hematology, Hanover Medical School, Carl-Neuberg-Str. 1, 30625, Hannover, Germany., Yang L; Cardiovascular Branch, National Heart Lung and Blood Institute, Bethesda, MD, 20892, USA.; Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA., Cao H; Cardiovascular Branch, National Heart Lung and Blood Institute, Bethesda, MD, 20892, USA., Jesus DF; Islet Cell and Regenerative Biology, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Stem Cell Institute, Harvard Medical School, Boston, 02215, MA, USA., Kulkarni RN; Islet Cell and Regenerative Biology, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Stem Cell Institute, Harvard Medical School, Boston, 02215, MA, USA., Zevnik B; CECAD in vivo Research Facility, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931, Cologne, Germany., Tröder SE; CECAD in vivo Research Facility, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931, Cologne, Germany., Knippschild U; Department of General and Visceral Surgery, University Hospital Ulm, Albert-Einstein Allee 93, 89081, Ulm, Germany., Edwards PA; Department of Biological Chemistry, University of California, Los Angeles (UCLA), 650 Charles E. Young Drive South, Los Angeles, CA, 90095, USA.; Department of Medicine, Division of Cardiology, UCLA, 650 Charles E. Young Drive South, Los Angeles, CA, 90095, USA., Lee RG; IONIS Pharmaceuticals, Carlsbad, CA, 92010, USA., Yamamoto M; Department of Medical Biochemistry, Tohoku Medical Megabank Organization, Sendai, 980-8573, Japan., Ulitsky I; Department of Biological Regulation, Weizmann Institute of Science, Rehovot, 76100, Israel., Fernandez-Rebollo E; Functional Genomics and Metabolism Unit, Department for Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, 5230, Odense M, Denmark., Vallim TQA; Department of Biological Chemistry, University of California, Los Angeles (UCLA), 650 Charles E. Young Drive South, Los Angeles, CA, 90095, USA. TVallim@mednet.ucla.edu.; Department of Medicine, Division of Cardiology, UCLA, 650 Charles E. Young Drive South, Los Angeles, CA, 90095, USA. TVallim@mednet.ucla.edu., Kornfeld JW; Functional Genomics and Metabolism Unit, Department for Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, 5230, Odense M, Denmark. janwilhelmkornfeld@bmb.sdu.dk.; Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931, Cologne, Germany. janwilhelmkornfeld@bmb.sdu.dk.; Cologne Cluster of Excellence-Cellular Stress Responses in Ageing-associated Diseases (CECAD), Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931, Cologne, Germany. janwilhelmkornfeld@bmb.sdu.dk. |
| المصدر: | Nature communications [Nat Commun] 2020 Jan 31; Vol. 11 (1), pp. 644. Date of Electronic Publication: 2020 Jan 31. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: [London] : Nature Pub. Group |
| مواضيع طبية MeSH: | Diabetes Mellitus, Type 2/*genetics , Glucose/*metabolism , Liver/*metabolism , MafG Transcription Factor/*genetics , Obesity/*genetics , RNA, Long Noncoding/*genetics , Repressor Proteins/*genetics, Aged ; Animals ; Diabetes Mellitus, Type 2/metabolism ; Humans ; MafG Transcription Factor/metabolism ; Male ; Mice ; Middle Aged ; Obesity/metabolism ; RNA, Long Noncoding/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Repressor Proteins/metabolism ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism |
| مستخلص: | Obesity and type 2 diabetes mellitus are global emergencies and long noncoding RNAs (lncRNAs) are regulatory transcripts with elusive functions in metabolism. Here we show that a high fraction of lncRNAs, but not protein-coding mRNAs, are repressed during diet-induced obesity (DIO) and refeeding, whilst nutrient deprivation induced lncRNAs in mouse liver. Similarly, lncRNAs are lost in diabetic humans. LncRNA promoter analyses, global cistrome and gain-of-function analyses confirm that increased MAFG signaling during DIO curbs lncRNA expression. Silencing Mafg in mouse hepatocytes and obese mice elicits a fasting-like gene expression profile, improves glucose metabolism, de-represses lncRNAs and impairs mammalian target of rapamycin (mTOR) activation. We find that obesity-repressed LincIRS2 is controlled by MAFG and observe that genetic and RNAi-mediated LincIRS2 loss causes elevated blood glucose, insulin resistance and aberrant glucose output in lean mice. Taken together, we identify a MAFG-lncRNA axis controlling hepatic glucose metabolism in health and metabolic disease. |
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| معلومات مُعتمدة: | K12 GM106996 United States GM NIGMS NIH HHS; K22 HL139921 United States HL NHLBI NIH HHS; ZIA HL006159 United States ImNIH Intramural NIH HHS; ZIA HL006103 United States ImNIH Intramural NIH HHS |
| المشرفين على المادة: | 0 (MAFG protein, human) 0 (MafG Transcription Factor) 0 (Mafg protein, mouse) 0 (RNA, Long Noncoding) 0 (RNA, Messenger) 0 (Repressor Proteins) EC 2.7.11.1 (TOR Serine-Threonine Kinases) IY9XDZ35W2 (Glucose) |
| تواريخ الأحداث: | Date Created: 20200202 Date Completed: 20200511 Latest Revision: 20211204 |
| رمز التحديث: | 20240628 |
| مُعرف محوري في PubMed: | PMC6994702 |
| DOI: | 10.1038/s41467-020-14323-y |
| PMID: | 32005828 |
| قاعدة البيانات: | MEDLINE |
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