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Giroud, M. ; Kotschi, S.* ; Kwon, Y. ; Le Thuc, O. ; Hoffmann, A. ; Gil Lozano, M. ; Karbiener, M.* ; Higareda-Almaraz, J. ; Khani, S. ; Tews, D.* ; Fischer-Posovszky, P.* ; Sun, W.* ; Dong, H.* ; Ghosh, A.* ; Wolfrum, C.* ; Wabitsch, M.* ; Virtanen, K.A.* ; Blüher, M. ; Nielsen, S.* ; Zeigerer, A. ; García-Cáceres, C. ; Scheideler, M. ; Herzig, S. ; Bartelt, A.

The obesity-linked human lncRNA AATBC stimulates mitochondrial function in adipocytes.

EMBO Rep. 24:e57600 (2023)
Verlagsversion DOI PMC
Open Access Hybrid
Creative Commons Lizenzvertrag
Adipocytes are critical regulators of metabolism and energy balance. While white adipocyte dysfunction is a hallmark of obesity-associated disorders, thermogenic adipocytes are linked to cardiometabolic health. As adipocytes dynamically adapt to environmental cues by functionally switching between white and thermogenic phenotypes, a molecular understanding of this plasticity could help improving metabolism. Here, we show that the lncRNA Apoptosis associated transcript in bladder cancer (AATBC) is a human-specific regulator of adipocyte plasticity. Comparing transcriptional profiles of human adipose tissues and cultured adipocytes we discovered that AATBC was enriched in thermogenic conditions. Using primary and immortalized human adipocytes we found that AATBC enhanced the thermogenic phenotype, which was linked to increased respiration and a more fragmented mitochondrial network. Expression of AATBC in adipose tissue of mice led to lower plasma leptin levels. Interestingly, this association was also present in human subjects, as AATBC in adipose tissue was inversely correlated with plasma leptin levels, BMI, and other measures of metabolic health. In conclusion, AATBC is a novel obesity-linked regulator of adipocyte plasticity and mitochondrial function in humans.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Adipocyte ; Mitochondrial Dynamics ; Non-coding Rna ; Obesity ; Thermogenesis; Brown Adipose-tissue; Glucose-homeostasis; Rna-seq; Thermogenesis; Localization; Adaptation; Fission; Reveals; Brite; Ucp1
Sprache englisch
Veröffentlichungsjahr 2023
HGF-Berichtsjahr 2023
ISSN (print) / ISBN 1469-221X
e-ISSN 1469-3178
Zeitschrift EMBO Reports
Quellenangaben Band: 24, Heft: 10, Seiten: , Artikelnummer: e57600 Supplement: ,
Verlag EMBO Press
Verlagsort 111 River St, Hoboken 07030-5774, Nj Usa
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Cancer (IDC)
Institute of Diabetes and Obesity (IDO)
Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
POF Topic(s) 90000 - German Center for Diabetes Research
30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-501900-251
G-501900-254
G-502200-001
G-506501-001
G-501900-252
G-501900-224
Förderungen EC | H2020 | PRIORITY 'Excellent science' | H2020 European Research Council (ERC)
Deutsches Zentrum für Herz-Kreislaufforschung (DZHK)
Deutsche Forschungsgemeinschaft (DFG)
Alexander von Humboldt-Stiftung (AvH)
Helmholtz Zentrum München (Helmholtz Centre Munich, German Research Center for Environmental Health)
DOI 10.15252/embr.202357600
WOS ID 001062915300001
Scopus ID 85169917394
PubMed ID 37671834
Erfassungsdatum 2023-10-18
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