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Cold-induced expression of a truncated adenylyl cyclase 3 acts as rheostat to brown fat function.

التفاصيل البيبلوغرافية
العنوان: Cold-induced expression of a truncated adenylyl cyclase 3 acts as rheostat to brown fat function.
المؤلفون: Khani S; Institute for Genetics, University of Cologne, Cologne, Germany.; Max Planck Institute for Metabolism Research, Cologne, Germany., Topel H; Department for Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark.; Novo Nordisk Foundation Center for Adipocyte Signaling (Adiposign), University of Southern Denmark, Odense, Denmark., Kardinal R; Institute of Innate Immunity, Medical Faculty, University of Bonn, Bonn, Germany., Tavanez AR; Department for Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark.; Novo Nordisk Foundation Center for Adipocyte Signaling (Adiposign), University of Southern Denmark, Odense, Denmark., Josephrajan A; Department for Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark.; Novo Nordisk Foundation Center for Adipocyte Signaling (Adiposign), University of Southern Denmark, Odense, Denmark., Larsen BDM; Department for Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark., Gaudry MJ; Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden., Leyendecker P; Institute of Innate Immunity, Medical Faculty, University of Bonn, Bonn, Germany., Egedal NM; Department for Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark.; Novo Nordisk Foundation Center for Adipocyte Signaling (Adiposign), University of Southern Denmark, Odense, Denmark., Güller AS; Department for Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark., Stanic N; Department for Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark.; Novo Nordisk Foundation Center for Adipocyte Signaling (Adiposign), University of Southern Denmark, Odense, Denmark., Ruppert PMM; Department for Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark., Gaziano I; Max Planck Institute for Metabolism Research, Cologne, Germany., Hansmeier NR; Max Planck Institute for Metabolism Research, Cologne, Germany., Schmidt E; Max Planck Institute for Metabolism Research, Cologne, Germany., Klemm P; Max Planck Institute for Metabolism Research, Cologne, Germany., Vagliano LM; Institute of Innate Immunity, Medical Faculty, University of Bonn, Bonn, Germany., Stahl R; Institute of Innate Immunity, Medical Faculty, University of Bonn, Bonn, Germany., Duthie F; Institute of Innate Immunity, Medical Faculty, University of Bonn, Bonn, Germany., Krause JH; Institute of Innate Immunity, Medical Faculty, University of Bonn, Bonn, Germany., Bici A; Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University, Munich, Germany., Engelhard CA; Department for Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark.; Centre for Physical Activity Research, Department of Infectious Diseases, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark., Gohlke S; Department of Adipocyte Development and Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke, Nuthetal, Germany., Frommolt P; Institute of Human Genetics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany., Gnad T; Institute of Pharmacology and Toxicology, University Hospital, University of Bonn, Bonn, Germany., Rada-Iglesias A; Institute of Biomedicine and Biotechnology of Cantabria (IBBTEC), CSIC/University of Cantabria, Santander, Spain., Pradas-Juni M; Novo Nordisk Foundation Center for Basic Metabolic Research (CBMR), Copenhagen, Denmark., Schulz TJ; Department of Adipocyte Development and Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke, Nuthetal, Germany.; German Center for Diabetes Research (DZD), München-Neuherberg, Germany., Wunderlich FT; Max Planck Institute for Metabolism Research, Cologne, Germany., Pfeifer A; Institute of Pharmacology and Toxicology, University Hospital, University of Bonn, Bonn, Germany., Bartelt A; Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University, Munich, Germany.; Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, German Research Center for Environmental Health, Neuherberg, Germany.; German Center for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany.; Department of Molecular Metabolism and Sabri Ülker Center for Metabolic Research, Harvard T.H. Chan School of Public Health, Boston, MA, USA., Jastroch M; Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden., Wachten D; Institute of Innate Immunity, Medical Faculty, University of Bonn, Bonn, Germany. dwachten@uni-bonn.de., Kornfeld JW; Department for Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark. janwilhelmkornfeld@bmb.sdu.dk.; Novo Nordisk Foundation Center for Adipocyte Signaling (Adiposign), University of Southern Denmark, Odense, Denmark. janwilhelmkornfeld@bmb.sdu.dk.
المصدر: Nature metabolism [Nat Metab] 2024 Jun; Vol. 6 (6), pp. 1053-1075. Date of Electronic Publication: 2024 Apr 29.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Springer Nature Country of Publication: Germany NLM ID: 101736592 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2522-5812 (Electronic) Linking ISSN: 25225812 NLM ISO Abbreviation: Nat Metab Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Berlin : Springer Nature, [2019]-
مواضيع طبية MeSH: Adenylyl Cyclases*/metabolism , Adenylyl Cyclases*/genetics , Adipose Tissue, Brown*/metabolism , Cold Temperature*, Animals ; Mice ; Male ; Humans ; Thermogenesis/genetics ; Energy Metabolism ; Cyclic AMP/metabolism ; Mice, Knockout
مستخلص: Promoting brown adipose tissue (BAT) activity innovatively targets obesity and metabolic disease. While thermogenic activation of BAT is well understood, the rheostatic regulation of BAT to avoid excessive energy dissipation remains ill-defined. Here, we demonstrate that adenylyl cyclase 3 (AC3) is key for BAT function. We identified a cold-inducible promoter that generates a 5' truncated AC3 mRNA isoform (Adcy3-at), whose expression is driven by a cold-induced, truncated isoform of PPARGC1A (PPARGC1A-AT). Male mice lacking Adcy3-at display increased energy expenditure and are resistant to obesity and ensuing metabolic imbalances. Mouse and human AC3-AT are retained in the endoplasmic reticulum, unable to translocate to the plasma membrane and lack enzymatic activity. AC3-AT interacts with AC3 and sequesters it in the endoplasmic reticulum, reducing the pool of adenylyl cyclases available for G-protein-mediated cAMP synthesis. Thus, AC3-AT acts as a cold-induced rheostat in BAT, limiting adverse consequences of cAMP activity during chronic BAT activation.
(© 2024. The Author(s), under exclusive licence to Springer Nature Limited.)
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معلومات مُعتمدة: 675014 EC | EC Seventh Framework Programm | FP7 Ideas: European Research Council (FP7-IDEAS-ERC - Specific Programme: "Ideas" Implementing the Seventh Framework Programme of the European Community for Research, Technological Development and Demonstration Activities (2007 to 2013)); PROTEOFIT EC | EC Seventh Framework Programm | FP7 Ideas: European Research Council (FP7-IDEAS-ERC - Specific Programme: "Ideas" Implementing the Seventh Framework Programme of the European Community for Research, Technological Development and Demonstration Activities (2007 to 2013)); 33444 Novo Nordisk Fonden (Novo Nordisk Foundation); 28416 Novo Nordisk Fonden (Novo Nordisk Foundation); A/12/97620 Deutscher Akademischer Austauschdienst (German Academic Exchange Service); TRR333/1 (450149205) Deutsche Forschungsgemeinschaft (German Research Foundation); SFB 1454 (432325352) Deutsche Forschungsgemeinschaft (German Research Foundation); TRR83 Deutsche Forschungsgemeinschaft (German Research Foundation); SPP1926 Deutsche Forschungsgemeinschaft (German Research Foundation); SPP1726 Deutsche Forschungsgemeinschaft (German Research Foundation); FOR2743 Deutsche Forschungsgemeinschaft (German Research Foundation); SFB1123-B10 Deutsche Forschungsgemeinschaft (German Research Foundation); 676-2021 European Molecular Biology Organization (EMBO)
المشرفين على المادة: EC 4.6.1.1 (Adenylyl Cyclases)
EC 4.6.1.1 (adenylate cyclase 3)
E0399OZS9N (Cyclic AMP)
تواريخ الأحداث: Date Created: 20240429 Date Completed: 20240625 Latest Revision: 20240715
رمز التحديث: 20240715
DOI: 10.1038/s42255-024-01033-8
PMID: 38684889
قاعدة البيانات: MEDLINE
الوصف
تدمد:2522-5812
DOI:10.1038/s42255-024-01033-8