Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 553, Issue -, Pages 30-36Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2021.03.064
Keywords
Capmatinib; AMPK; Irisin; Adipocyte; Lipogenesis; Lipolysis
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Funding
- National Research Foundation of Korea (NRF) - Korea government (MSIT) [2019R1A2C4070189]
- Chung-Ang Research Scholarship
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CAP can attenuate lipogenesis and enhance lipolysis in adipocytes through the irisin/AMPK pathway, suggesting that it may be a novel therapeutic agent for obesity.
Recently, there is a rapid increase in the incidence of obesity, a condition for which there are no effective therapeutic agents. Capmatinib (CAP), a novel mesenchymal-to-epithelial transition inhibitor, is reported to attenuate pro-inflammatory mediators and oxidative stress. In this study, the effects of CAP on lipo-genesis in the adipocytes were examined. Treatment with CAP dose-dependently suppressed lipid accumulation in, and differentiation of, and increased lipolysis in, 3T3-L1 adipocytes. Additionally, CAP treatment augmented adenosine monophosphate-activated protein kinase (AMPK) phosphorylation and FNDC5 expression in the adipocytes. Transfection with si-AMPK or si-FNDC5 mitigated the CAP-induced suppression of lipogenesis and enhanced lipolysis. Furthermore, transfection with si-FNDC5 mitigated the CAP-induced phosphorylation of AMPK. These results suggest that the anti-obesity effect of CAP is mediated through the irisin/AMPK pathway and that CAP is a novel therapeutic agent for obesity. (c) 2021 Elsevier Inc. All rights reserved.
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