Creatine kinase B regulates glycolysis and <i>de novo</i> lipogenesis pathways to control lipid accumulation during adipogenesis. 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. Cell Reports, 44(11):116489, November, 2025. ![Creatine kinase B regulates glycolysis and <i>de novo</i> lipogenesis pathways to control lipid accumulation during adipogenesis [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex 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.
@article{renzi_creatine_2025,
title = {Creatine kinase {B} regulates glycolysis and \textit{de novo} lipogenesis pathways to control lipid accumulation during adipogenesis},
volume = {44},
issn = {2211-1247},
url = {https://www.sciencedirect.com/science/article/pii/S2211124725012604},
doi = {10.1016/j.celrep.2025.116489},
abstract = {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.},
number = {11},
urldate = {2025-11-14},
journal = {Cell Reports},
author = {Renzi, Gianluca and Higos, Romane and Vlassakev, Ivan and Bello, Abdoul Akim and Omar-Hmeadi, Muhmmad and Hansen, Mattias and Merabtene, Fatiha and Rouault, Christine and Hodek, Ondrej and Massier, Lucas and Antonny, Bruno and Marcelin, Geneviève and Rahbani, Janane F. and Lecoutre, Simon and Maqdasy, Salwan},
month = nov,
year = {2025},
keywords = {AKT-mTORC, CKB, ChREBP, adipogenesis, creatine kinase, lipogenesis, white adipocyte},
pages = {116489},
}
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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. 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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. 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