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Renzi, G.* ; Higos, R.* ; Vlassakev, I.* ; Bello, A.A.* ; Omar-Hmeadi, M.* ; Hansen, M.* ; Merabtene, F.* ; Rouault, C.* ; Hodek, O.* ; Massier, L. ; Antonny, B.* ; Marcelin, G.* ; Rahbani, J.F.* ; Lecoutre, S.* ; Maqdasy, S.*

Creatine kinase B regulates glycolysis and de novo lipogenesis pathways to control lipid accumulation during adipogenesis.

Cell Rep. 44, 22:116489 (2025)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
White adipocyte differentiation or adipogenesis requires coordination of metabolic sensing and transcriptional modifications to orchestrate lipid storage. Creatine and its kinases are implicated in adipose energy buffering, but the roles of cytosolic (CKB) and mitochondrial (CKMT2) creatine kinases in adipogenesis are unclear. We find that both CKB and CKMT2 are progressively upregulated during differentiation. Functional studies show that CKB restrains de novo lipogenesis (DNL) by limiting activation of carbohydrate-responsive element-binding protein (ChREBP), a key regulator of lipogenic genes. Mechanistically, CKB interacts with AKT and regulates its activation in response to insulin. Loss of CKB causes persistent AKT-mTORC1 signaling, increases glycolytic flux, and enhances ChREBP activation, thereby promoting glucose-derived lipid synthesis. Thus, CKB acts as a metabolic rheostat linking creatine-kinase activity to insulin signaling and nutrient-responsive transcription. We propose a CKB-AKT-ChREBP regulatory axis that contributes to metabolic remodeling and lipid homeostasis during adipocyte differentiation.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Akt-mtorc ; Ckb ; Cp: Metabolism ; Chrebp ; Adipogenesis ; Creatine Kinase ; De Novo Lipogenesis ; White Adipocyte; Creatine Supplementation Prevents; Depot-specific Differences; Diet-induced Obesity; De-novo Lipogenesis; Adipose-tissue; Human Adipocyte; Insulin-resistance; Mammalian Protein; Gene-expression; Fatty Liver
Sprache englisch
Veröffentlichungsjahr 2025
HGF-Berichtsjahr 2025
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Zeitschrift Cell Reports
Quellenangaben Band: 44, Heft: 11, Seiten: 22, Artikelnummer: 116489 Supplement: ,
Verlag Cell Press
Verlagsort 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
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-506509-001
Förderungen CIMED, European Foundation for the Study of Diabetes Rising Star award
Swedish Research Council
French National Agency for Research
European Research Council (ERC Synergy grant SPHERES)
WOS ID 001613659100001
DOI 10.1016/j.celrep.2025.116489
PubMed ID 41196679
Erfassungsdatum 2025-11-07
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