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Wu, C.* ; Wang, T.* ; Ghosh, A.* ; Long, F.* ; Sharma, A.K.* ; Dahlby, T.* ; Noé, F.* ; Severi, I.* ; Colleluori, G.* ; Cinti, S.* ; Giordano, A.* ; Ding, L.* ; Khandelwal, R.* ; Kostidis, S.* ; Giera, M.* ; Balázová, L.* ; Gardeux, V.* ; Abu-Nawwas, L.* ; Deplancke, B.* ; Chourasia, S.* ; Kleiner, S.* ; Hamilton, B.S.* ; Alcántara, J.M.A.* ; Ruiz, J.R.* ; Blüher, M. ; Pekcec, A.* ; Balaz, M.* ; Gross, A.* ; Neubauer, H.* ; Wolfrum, C.*

MTCH2 modulates CPT1 activity to regulate lipid metabolism of adipocytes.

Nat. Commun. 16, 18:8831 (2025)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Metabolic disorders, including obesity and metabolic-associated steatohepatitis, arise from a chronic energy surplus. Thus, enhancing energy dissipation through increased respiration holds significant therapeutic potential for metabolic disorders. Through a comprehensive analysis of human and murine adipose tissues, along with a functional screen, we identify mitochondrial carrier homolog 2, a mitochondrial outer membrane protein, as a pivotal regulator of mitochondrial metabolism. Intriguingly, its expression in adipose tissue is a strong determinant of obesity in humans. Adipocyte-specific ablation of mitochondrial carrier homolog 2 improves mitochondrial function and whole-body energy expenditure, independent of uncoupling protein 1. Furthermore, mitochondrial carrier homolog 2 regulates mitochondrial influx of free fatty acids by modulating the sensitivity of carnitine palmitoyltransferase 1 to malonyl-CoA through direct physical interaction, leading to enhanced energy expenditure in adipocytes/adipose tissue. Here we show mitochondrial carrier homolog 2 functions as a negative regulator of energy metabolism in adipocytes and represents a potential target for treating obesity and related metabolic disorders.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Brown Adipose-tissue; Beige; Phosphorylation; Thermogenesis; Transport; Brite; Cells; Cold
Sprache englisch
Veröffentlichungsjahr 2025
HGF-Berichtsjahr 2025
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 16, Heft: 1, Seiten: 18, Artikelnummer: 8831 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
POF Topic(s) 30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-506501-001
Förderungen Boehringer Ingelheim
European Union's Horizon 2020 research and innovation program under the Marie Sklodowska-Curie grant
Slovak Research and Development Agency
VEGA
Spanish Ministry of Education
MICIU/AEI
ESF+
DOI 10.1038/s41467-025-63880-7
WOS ID 001587519800027
Scopus ID 105017653060
PubMed ID 41044057
Erfassungsdatum 2025-10-15
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